@article{MTMT:35195205,
	title = {LPA suppresses HLA-DR expression in human melanoma cells: a potential immune escape mechanism involving LPAR1 and DR6-mediated release of IL-10},
	url = {https://m2.mtmt.hu/api/publication/35195205},
	author = {Major, Enikő and Lin, Kuan-Hung and Lee, Sue Chin and Káldi, Krisztina and Győrffy, Balázs and Tigyi, Gabor and Benyó, Zoltán},
	doi = {10.1038/s41401-024-01373-x},
	journal-iso = {ACTA PHARMACOL SIN},
	journal = {ACTA PHARMACOLOGICA SINICA},
	volume = {46},
	unique-id = {35195205},
	issn = {1671-4083},
	abstract = {While immune checkpoint inhibitors (ICIs) are promising in the treatment of metastatic melanoma, about half of patients do not respond well to them. Low levels of human leukocyte antigen-DR (HLA-DR) in tumors have been shown to negatively influence prognosis and response to ICIs. Lysophosphatidic acid (LPA) is produced in large amounts by melanoma and is abundantly present in the tumor microenvironment. LPA induces the release of various cytokines and chemokines from tumor cells, which affect cancer development, metastasis, and tumor immunity. In the present study, we investigated the role of LPA-induced IL-10 release in regulating HLA-DR expression and the underlying mechanisms in human melanoma cells. We showed that LPA (0.001–10 μM) dose-dependently increased DR6 transcript levels through activating LPAR1 in HEK293T cells. Knockdown of NF-κB1 abrogated the LPA-increased DR6 expression without affecting basal DR6 expression in both A2058 and A375 melanoma cell lines. LPA (10 µM) significantly increased IL-10 transcripts in A2058 and A375 melanoma cells, the effect was abolished by pharmacological inhibition of LPAR1 or knockdown of DR6. We found a statistically significant correlation between the expression of LPAR1, DR6 and IL-10 in human melanoma tissue and an association between increased expression of LPAR1 and reduced effectiveness of ICI therapy. We demonstrated that LPA (10 µM) markedly suppressed HLA-DR expression in both A375 and A2058 melanoma cells via activating the LPAR1-DR6-IL-10 pathway. These data suggest that the LPAR1-DR6-IL-10 autocrine loop could constitute a novel mechanism used by tumor cells to evade immunosurveillance by decreasing HLA-DR expression.},
	year = {2025},
	eissn = {1745-7254},
	pages = {222-230},
	orcid-numbers = {Major, Enikő/0000-0001-5854-9395; Káldi, Krisztina/0000-0002-5724-0182; Győrffy, Balázs/0000-0002-5772-3766; Tigyi, Gabor/0000-0001-5371-171X; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:34942326,
	title = {Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells},
	url = {https://m2.mtmt.hu/api/publication/34942326},
	author = {Balijepalli, Pravita and Knode, Brianna K. and Nahulu, Samuel A. and Abrahamson, Emily L. and Nivison, Mary P. and Meier, Kathryn E.},
	doi = {10.1002/ccs3.12019},
	journal-iso = {J CELL COMMUN SIGNAL},
	journal = {JOURNAL OF CELL COMMUNICATION AND SIGNALING},
	volume = {18},
	unique-id = {34942326},
	issn = {1873-9601},
	keywords = {FAMILY; gender; SPACE; inequality; COVID-19},
	year = {2024},
	eissn = {1873-961X},
	orcid-numbers = {Balijepalli, Pravita/0000-0001-8096-1319}
}

@article{MTMT:34942324,
	title = {Phosphoproteomics Reveals Selective Regulation of Signaling Pathways by Lysophosphatidic Acid Species in Macrophages},
	url = {https://m2.mtmt.hu/api/publication/34942324},
	author = {Dietze, Raimund and Szymanski, Witold and Ojasalu, Kaire and Finkernagel, Florian and Nist, Andrea and Stiewe, Thorsten and Graumann, Johannes and Mueller, Rolf},
	doi = {10.3390/cells13100810},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {13},
	unique-id = {34942324},
	keywords = {MACROPHAGES; phosphoproteomics; Lysophosphatidic acid; cholesterol biosynthesis; RHO/RAC1 signaling},
	year = {2024},
	eissn = {2073-4409},
	orcid-numbers = {Graumann, Johannes/0000-0002-3015-5850}
}

@article{MTMT:34904147,
	title = {Linking the Autotaxin-LPA Axis to Medicinal Cannabis and the Endocannabinoid System},
	url = {https://m2.mtmt.hu/api/publication/34904147},
	author = {Eymery, Mathias C. and Boumendjel, Ahcene and McCarthy, Andrew A. and Hausmann, Jens},
	doi = {10.3390/ijms25063212},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34904147},
	issn = {1661-6596},
	keywords = {CANNABINOIDS; endocannabinoid; Lysophosphatidic acid; tetrahydrocannabinol; AUTOTAXIN},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Boumendjel, Ahcene/0000-0002-1830-6409}
}

@article{MTMT:34942322,
	title = {Discovery of potent chromone-based autotaxin inhibitors inspired by cannabinoids},
	url = {https://m2.mtmt.hu/api/publication/34942322},
	author = {Eymery, Mathias Christophe and Nguyen, Kim-Anh and Basu, Shibom and Hausmann, Jens and Tran-Nguyen, Viet-Khoa and Seidel, Hans Peter and Gutierrez, Lola and Boumendjel, Ahcene and McCarthy, Andrew Aloysius},
	doi = {10.1016/j.ejmech.2023.115944},
	journal-iso = {EUR J MED CHEM},
	journal = {EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY},
	volume = {263},
	unique-id = {34942322},
	issn = {0223-5234},
	keywords = {INHIBITORS; Indoles; molecular modelling; Chromones; cannabinoid; Structural biology; AUTOTAXIN; macromolecular X-ray crystallography},
	year = {2024},
	eissn = {1768-3254},
	orcid-numbers = {Basu, Shibom/0000-0001-6484-8236; Tran-Nguyen, Viet-Khoa/0000-0001-7497-333X; Boumendjel, Ahcene/0000-0002-1830-6409}
}

@article{MTMT:35305972,
	title = {Lysophosphatidic acid metabolism and signaling in heart disease},
	url = {https://m2.mtmt.hu/api/publication/35305972},
	author = {Jose, Anu and Fernando, Jeffy J. and Kienesberger, Petra C.},
	doi = {10.1139/cjpp-2024-0077},
	journal-iso = {CAN J PHYSIOL PHARM},
	journal = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
	unique-id = {35305972},
	issn = {0008-4212},
	keywords = {heart disease; CARDIOMYOPATHY; Lysophosphatidic acid; AUTOTAXIN; lipid phosphate phosphatase},
	year = {2024},
	eissn = {1205-7541}
}

@article{MTMT:34942325,
	title = {Discovery of the Novel, Orally Active, and Selective LPA1 Receptor Antagonist ACT-1016-0707 as a Preclinical Candidate for the Treatment of Fibrotic Diseases},
	url = {https://m2.mtmt.hu/api/publication/34942325},
	author = {Lescop, Cyrille and Birker, Magdalena and Brotschi, Christine and Burki, Cedric and Morrison, Keith and Froidevaux, Sylvie and Delahaye, Stephane and Nayler, Oliver and Bolli, Martin H.},
	doi = {10.1021/acs.jmedchem.3c01827},
	journal-iso = {J MED CHEM},
	journal = {JOURNAL OF MEDICINAL CHEMISTRY},
	volume = {67},
	unique-id = {34942325},
	issn = {0022-2623},
	year = {2024},
	eissn = {1520-4804},
	pages = {2397-2424},
	orcid-numbers = {Birker, Magdalena/0000-0001-7995-9465; Burki, Cedric/0009-0007-9108-9483}
}

@article{MTMT:35659807,
	title = {The effect of lysophosphatidic acid on myometrial contractility and the mRNA transcription of its receptors in the myometrium at different stages of endometrosis in mares},
	url = {https://m2.mtmt.hu/api/publication/35659807},
	author = {Piotrowska-Tomala, Katarzyna Karolina and Szóstek-Mioduchowska, Anna and Jonczyk, Agnieszka Walentyna and Drzewiecka, Ewa Monika and Wrobel, Michał Hubert and Hojo, Takuo and Ferreira-Dias, Graca and Skarzynski, Dariusz Jan},
	doi = {10.1186/s12917-024-04384-2},
	journal-iso = {BMC VET RES},
	journal = {BMC VETERINARY RESEARCH},
	volume = {20},
	unique-id = {35659807},
	issn = {1746-6148},
	year = {2024},
	eissn = {1746-6148}
}

@article{MTMT:34282715,
	title = {Role of enterocyte Enpp2 and autotaxin in regulating lipopolysaccharide levels, systemic inflammation, and atherosclerosis},
	url = {https://m2.mtmt.hu/api/publication/34282715},
	author = {Chattopadhyay, Arnab and Mukherjee, Pallavi and Sulaiman, Dawoud and Wang, Huan and Girjalva, Victor and Dorreh, Nasrin and Jacobs, Jonathan P. and Delk, Samuel and Moolenaar, Wouter H. and Navab, Mohamad and Reddy, Srinivasa T. and Fogelman, Alan M.},
	doi = {10.1016/j.jlr.2023.100370},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {64},
	unique-id = {34282715},
	issn = {0022-2275},
	abstract = {Conversion of lysophosphatidylcholine to lysophosphatidic acid (LPA) by autotaxin, a secreted phospholipase D, is a major pathway for producing LPA. We previously reported that feeding Ldlr-/- mice standard mouse chow supplemented with un-saturated LPA or lysophosphatidylcholine qualita-tively mimicked the dyslipidemia and atherosclerosis induced by feeding a Western diet (WD). Here, we report that adding unsaturated LPA to standard mouse chow also increased the content of reactive oxygen species and oxidized phospholipids (OxPLs) in jejunum mucus. To determine the role of intestinal autotaxin, enterocyte-specific Ldlr-/-/Enpp2 KO (in-testinal KO) mice were generated. In control mice, the WD increased enterocyte Enpp2 expression and raised autotaxin levels. Ex vivo, addition of OxPL to jejunum from Ldlr-/- mice on a chow diet induced expression of Enpp2. In control mice, the WD raised OxPL levels in jejunum mucus and decreased gene expression in enterocytes for a number of peptides and proteins that affect antimicrobial activity. On the WD, the control mice developed elevated levels of lipopolysaccharide in jejunum mucus and plasma, with increased dyslipidemia and increased athero-sclerosis. All these changes were reduced in the in-testinal KO mice. We conclude that the WD increases the formation of intestinal OxPL, which i) induce enterocyte Enpp2 and autotaxin resulting in higher enterocyte LPA levels; that ii) contribute to the formation of reactive oxygen species that help to maintain the high OxPL levels; iii) decrease intestinal antimicrobial activity; and iv) raise plasma lipopoly-saccharide levels that promote systemic inflammation and enhance atherosclerosis.},
	keywords = {ATHEROSCLEROSIS; Small intestine; oxidized phospholipids; Lysophosphatidic acid; Lysophospholipase D; apolipoprotein A-I mimetic peptides; transgenic tomatoes expressing the apoA-I mimetic peptide 6F},
	year = {2023},
	eissn = {1539-7262},
	orcid-numbers = {Wang, Huan/0000-0003-1115-143X}
}

@article{MTMT:33856644,
	title = {Pathogenesis and Treatment of Pruritus Associated with Chronic Kidney Disease and Cholestasis},
	url = {https://m2.mtmt.hu/api/publication/33856644},
	author = {Kim, Jin-Cheol and Shim, Won-Sik and Kwak, In-Suk and Lee, Dong-Hun and Park, Jin-Seo and Lee, So-Yeon and Kang, Seok-Young and Chung, Bo-Young and Park, Chun-Wook and Kim, Hye-One},
	doi = {10.3390/ijms24021559},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33856644},
	issn = {1661-6596},
	abstract = {Itching is an unpleasant sensation that provokes the desire to scratch. In general, itching is caused by dermatologic diseases, but it can also be caused by systemic diseases. Since itching hampers patients' quality of life, it is important to understand the appropriate treatment and pathophysiology of pruritus caused by systemic diseases to improve the quality of life. Mechanisms are being studied through animal or human studies, and various treatments are being tested through clinical trials. We report current trends of two major systemic diseases: chronic kidney disease and cholestatic liver disease. This review summarizes the causes and pathophysiology of systemic diseases with pruritus and appropriate treatments. This article will contribute to patients' quality of life. Further research will help understand the mechanisms and develop new strategies in the future.},
	keywords = {chronic kidney disease; pruritus; Cholestasis; systemic disease},
	year = {2023},
	eissn = {1422-0067}
}

@article{MTMT:34343001,
	title = {Biomarkers in the Pathogenesis, Diagnosis, and Treatment of Systemic Sclerosis},
	url = {https://m2.mtmt.hu/api/publication/34343001},
	author = {Muruganandam, Maheswari and Ariza-Hutchinson, Angie and Patel, Rosemina A. and Sibbitt, Wilmer L.},
	doi = {10.2147/JIR.S379815},
	journal-iso = {J INFLAMM RES},
	journal = {JOURNAL OF INFLAMMATION RESEARCH},
	volume = {16},
	unique-id = {34343001},
	abstract = {Systemic sclerosis (SSc) is a complex autoimmune disease characterized by vascular damage, vasoinstability, and decreased perfusion with ischemia, inflammation, and exuberant fibrosis of the skin and internal organs. Biomarkers are analytic indicators of the biological and disease processes within an individual that can be accurately and reproducibly measured. The field of biomarkers in SSc is complex as recent studies have implicated at least 240 pathways and dysregulated proteins in SSc pathogenesis. Anti-nuclear antibodies (ANA) are classical biomarkers with well-described clinical classifications and are present in more than 90% of SSc patients and include anti-centromere, anti-Th/To, anti-RNA polymerase III, and anti-topoisomerase I antibodies. Transforming growth factor-beta (TGF-beta) is central to the fibrotic process of SSc and is intimately intertwined with other biomarkers. Tyrosine kinases, interferon-1 signaling, IL-6 signaling, endogenous thrombin, peroxisome proliferator-activated receptors (PPARs), lysophosphatidic acid receptors, and amino acid metabolites are new biomarkers with the potential for developing new therapeutic agents. Other biomarkers implicated in SSc-ILD include signal transducer and activator of transcription 4 (STAT4), CD226 (DNAX accessory molecule 1), interferon regulatory factor 5 (IRF5), interleukin-1 receptor-associated kinase-1 (IRAK1), connective tissue growth factor (CTGF), pyrin domain containing 1 (NLRP1), T-cell surface glycoprotein zeta chain (CD3 zeta) or CD247, the NLR family, SP-D (surfactant protein), KL-6, leucine-rich alpha 2-glycoprotein-1 (LRG1), CCL19, genetic factors including DRB1 alleles, the interleukins (IL-1, IL-4, IL-6, IL-8, IL-10 IL-13, IL-16, IL-17, IL-18, IL-22, IL-32, and IL-35), the chemokines CCL (2,3,5,13,20,21,23), CXC (8,9,10,11,16), CX3CL1 (fractalkine), and GDF15. Adiponectin (an indicator of PPAR activation) and maresin 1 are reduced in SSc patients. A new trend has been the use of biomarker panels with combined complex multifactor analysis, machine learning, and artificial intelligence to determine disease activity and response to therapy. The present review is an update of the various biomarker molecules, pathways, and receptors involved in the pathology of SSc.},
	keywords = {cytokine; autoantibody; scleroderma; systemic sclerosis; biomarker},
	year = {2023},
	eissn = {1178-7031},
	pages = {4633-4660}
}

@article{MTMT:33876434,
	title = {Treatment with lysophosphatidic acid prevents microglial activation and depression-like behaviours in a murine model of neuropsychiatric systemic lupus erythematosus},
	url = {https://m2.mtmt.hu/api/publication/33876434},
	author = {Nagata, Wataru and Koizumi, Akiho and Nakagawa, Keiichi and Takahashi, Sayaka and Gotoh, Mari and Satoh, Yasushi and Ishizuka, Toshiaki},
	doi = {10.1093/cei/uxad010},
	journal-iso = {CLIN EXP IMMUNOL},
	journal = {CLINICAL AND EXPERIMENTAL IMMUNOLOGY},
	volume = {212},
	unique-id = {33876434},
	issn = {0009-9104},
	abstract = {Novel therapeutic options for NPSLE are needed. MRL/lpr mice had significantly increased indices of depressive-like behaviours and expression of microglia or activated microglia in the brain compared to MRL/+ mice, and the increased expression was significantly suppressed by LPA treatment. LPA may regulate microglial activation, which is important in the pathogenesis of NPSLE, as well as blood-brain-barrier weakening and depression-like behaviours.Neuropsychiatric systemic lupus erythematosus (NPSLE) is an incurable disease characterised by neuropsychiatric symptoms, particularly depression. Novel therapeutic options for NPSLE are urgently needed. Several previous reports have suggested that both microglial activation and impaired neurogenesis may be involved in the progression of depression. In contrast, the administration of lysophosphatidic acid (LPA) ameliorates depression and anxiety. Therefore, in the present study, we determined whether treatment with LPA affects microglial activation, impaired neurogenesis, and abnormal behaviour in MRL/lpr mice. In both tail suspension test and forced swim test, the MRL/lpr mice exhibited a significant increase in total immobility time compared with MRL/+ mice. Treatment with LPA significantly suppressed the prolonged immobility time in MRL/lpr mice. In contrast, pretreatment with ki16425 (a specific antagonist of LPA receptor 1 and 3) significantly reversed the effects of LPA. Furthermore, MRL/lpr mice exhibited impairments in spatial working memory and visual cognitive memory, which were suppressed by LPA treatment. The expression levels of TMEM119, CD68, GFAP, and caspase-3 in the hippocampus and prefrontal cortex of MRL/lpr mice were significantly higher than those in MRL/+ mice. Treatment with LPA inhibited these increases in MRL/lpr mice. Pretreatment with ki16425 reversed LPA-mediated inhibition of microglial activation. The quantity of sodium fluorescein that leaked into the brain tissues in MRL/lpr mice were significantly higher than that in MRL/+ mice. Treatment with LPA tended to decrease the sodium fluorescein leakage. These findings suggest that treatment with LPA may regulate microglial activation, which is important in the pathogenesis of NPSLE, as well as blood-brain-barrier weakening and abnormal behaviour.},
	keywords = {DEPRESSION; neuroinflammation; microglia; LPA; NPSLE},
	year = {2023},
	eissn = {1365-2249},
	pages = {81-92},
	orcid-numbers = {Nagata, Wataru/0000-0002-4343-8315}
}

@article{MTMT:34282714,
	title = {Differential targeting of lysophosphatidic acid LPA1, LPA2, and LPA3 receptor signalling by tricyclic and tetracyclic antidepressants.},
	url = {https://m2.mtmt.hu/api/publication/34282714},
	author = {Olianas, Maria C. and Dedoni, Simona and Onali, Pierluigi},
	doi = {10.1016/j.ejphar.2023.176064},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {959},
	unique-id = {34282714},
	issn = {0014-2999},
	abstract = {We previously reported that in different cell types antidepressant drugs activate lysophosphatidic acid (LPA) LPA1 receptor to induce proliferative and prosurvival responses. Here, we further characterize this unique action of antidepressants by examining their effects on two additional LPA receptor family members, LPA2 and LPA3. Human LPA1-3 receptors were stably expressed in HEK-293 cells (HEK-LPA1,-LPA2 and -LPA3 cells) and their functional activity was determined by Western blot and immunofluorescence. LPA effectively stimulated the phosphorylation of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in HEK-LPA1,-LPA2, and-LPA3 cells. The tricyclic antidepressants amitriptyline, clomipramine, imipramine and desipramine increased phospho-ERK1/2 levels in HEK-LPA1 and -LPA3 cells but were relatively poor agonists in LPA2-expressing cells. The tetracyclic antidepressants mianserin and mirtazapine were active at all three LPA receptors. When combined with LPA, both amitriptyline and mianserin potentiated Gi/o-mediated phosphorylation of ERK1/2 induced by LPA in HEK-LPA1,-LPA2 and-LPA3 cells, CHO-K1 fibroblasts and HT22 hippocampal neuroblasts. This potentiation was associated with enhanced phosphorylation of CREB and S6 ribosomal protein, two molecular targets of activated ERK1/2. The antidepressants also potentiated LPA-induced Gq/11-mediated phosphorylation of AMP-activated protein kinase in HEK-LPA1 and -LPA3 cells. Conversely, amitriptyline and mianserin were found to inhibit LPA-induced Rho activation in HEK-LPA1 and LPA2 cells. These results indicate that tricyclic and tetracyclic antidepressants can act on LPA1, LPA2 and LPA3 receptor subtypes and exert differential effects on LPA signalling through these receptors.},
	keywords = {Antidepressants; Receptor signalling; HEK-293 cells; Human LPA receptors},
	year = {2023},
	eissn = {1879-0712}
}

@article{MTMT:34942318,
	title = {Autotaxin and Lysophosphatidic Acid Signalling: the Pleiotropic Regulatory Network in Cancer},
	url = {https://m2.mtmt.hu/api/publication/34942318},
	author = {Vit, Ondrez and Petrak, Jiri},
	doi = {10.14712/fb2023069050149},
	journal-iso = {FOLIA BIOL-PRAGUE},
	journal = {FOLIA BIOLOGICA},
	volume = {69},
	unique-id = {34942318},
	issn = {0015-5500},
	keywords = {CANCER; signal transduction; Lysophosphatidic acid; LPA; AUTOTAXIN; ENPP2},
	year = {2023},
	eissn = {0015-5500},
	pages = {149-162}
}

@article{MTMT:33231833,
	title = {Structure of the active G(i)-coupled human lysophosphatidic acid receptor 1 complexed with a potent agonist},
	url = {https://m2.mtmt.hu/api/publication/33231833},
	author = {Akasaka, Hiroaki and Tanaka, Tatsuki and Sano, Fumiya K. and Matsuzaki, Yuma and Shihoya, Wataru and Nureki, Osamu},
	doi = {10.1038/s41467-022-33121-2},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {13},
	unique-id = {33231833},
	issn = {2041-1723},
	abstract = {Lysophosphatidic acid receptor 1 (LPA(1)) is one of the six G protein-coupled receptors activated by the bioactive lipid, lysophosphatidic acid (LPA). LPA(1) is a drug target for various diseases, including cancer, inflammation, and neuropathic pain. Notably, LPA(1) agonists have potential therapeutic value for obesity and urinary incontinence. Here, we report a cryo-electron microscopy structure of the active human LPA(1)-G(i) complex bound to ONO-0740556, an LPA analog with more potent activity against LPA(1). Our structure elucidated the details of the agonist binding mode and receptor activation mechanism mediated by rearrangements of transmembrane segment 7 and the central hydrophobic core. A structural comparison of LPA(1) and other phylogenetically-related lipid-sensing GPCRs identified the structural determinants for lipid preference of LPA(1). Moreover, we characterized the structural polymorphisms at the receptor-G-protein interface, which potentially reflect the G-protein dissociation process. Our study provides insights into the detailed mechanism of LPA(1) binding to agonists and paves the way toward the design of drug-like agonists targeting LPA(1).LPA(1) is one of the GPCRs that are drug targets for various diseases. Here the authors report a cryo-EM structure of the active human LPA(1)-G(i) complex bound to an LPA analog with more potent activity against LPA(1) and clarified the ligand recognition mechanism.},
	year = {2022},
	eissn = {2041-1723},
	orcid-numbers = {Shihoya, Wataru/0000-0003-4813-5740; Nureki, Osamu/0000-0003-1813-7008}
}

@article{MTMT:33008121,
	title = {Glucagon-like Peptide-1 Secretion Is Inhibited by Lysophosphatidic Acid},
	url = {https://m2.mtmt.hu/api/publication/33008121},
	author = {Fernandes, Maria F. and Tomczewski, Michelle V and Duncan, Robin E.},
	doi = {10.3390/ijms23084163},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33008121},
	issn = {1661-6596},
	abstract = {Glucagon-like peptide-1 (GLP-1) potentiates glucose-stimulated insulin secretion (GSIS). While dozens of compounds stimulate GLP-1 secretion, few inhibit. Reduced GLP-1 secretion and impaired GSIS occur in chronic inflammation. Lysophosphatidic acids (LPAs) are bioactive phospholipids elevated in inflammation. The aim of this study was to test whether LPA inhibits GLP-1 secretion in vitro and in vivo. GLUTag L-cells were treated with various LPA species, with or without LPA receptor (LPAR) antagonists, and media GLP-1 levels, cellular cyclic AMP and calcium ion concentrations, and DPP4 activity levels were analyzed. Mice were injected with LPA, with or without LPAR antagonists, and serum GLP-1 and DPP4 activity were measured. GLUTag GLP-1 secretion was decreased similar to 70-90% by various LPAs. GLUTag expression of Lpar1, 2, and 3 was orders of magnitude higher than Lpar4, 5, and 6, implicating the former group in this effect. In agreement, inhibition of GLP-1 secretion was reversed by the LPAR1/3 antagonist Ki16425, the LPAR1 antagonists AM095 and AM966, or the LPAR2 antagonist LPA2-antagonist 1. We hypothesized involvement of G alpha(i)-mediated LPAR activity, and found that intracellular cyclic AMP and calcium ion concentrations were decreased by LPA, but restored by Ki16425. Mouse LPA injection caused an similar to 50% fall in circulating GLP-1, although only LPAR1 or LPAR1/3 antagonists, but not LPAR2 antagonism, prevented this. GLUTag L-cell and mouse serum DPP4 activity was unchanged by LPA or LPAR antagonists. LPA therefore impairs GLP-1 secretion in vitro and in vivo through G alpha(i)-coupled LPAR1/3 signaling, providing a new mechanism linking inflammation with impaired GSIS.},
	keywords = {Inflammation; Lysophosphatidic acid; Glucagon-Like Peptide 1; L-cells},
	year = {2022},
	eissn = {1422-0067}
}

@article{MTMT:32695273,
	title = {Lysophosphatidic Acid Promotes the Expansion of Cancer Stem Cells via TRPC3 Channels in Triple-Negative Breast Cancer},
	url = {https://m2.mtmt.hu/api/publication/32695273},
	author = {Hirata, N. and Yamada, S. and Yanagida, S. and Ono, A. and Yasuhiko, Y. and Nishida, M. and Kanda, Y.},
	doi = {10.3390/ijms23041967},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32695273},
	issn = {1661-6596},
	year = {2022},
	eissn = {1422-0067}
}

@article{MTMT:33008122,
	title = {Mesenteric Adipose Tissue Contributes to Intestinal Fibrosis in Crohn's Disease Through the ATX-LPA Axis},
	url = {https://m2.mtmt.hu/api/publication/33008122},
	author = {Huang, Liangyu and Qian, Wenwei and Xu, Yihan and Guo, Zhen and Yin, Yi and Guo, Feilong and Zhu, Weiming and Li, Yi},
	doi = {10.1093/ecco-jcc/jjac017},
	journal-iso = {J CROHNS COLITIS},
	journal = {JOURNAL OF CROHNS & COLITIS},
	unique-id = {33008122},
	issn = {1873-9946},
	abstract = {Background and Aims Intestinal fibrostenosis is an important cause of surgical intervention in patients with Crohn's disease [CD]. Hypertrophic mesenteric adipose tissue [MAT] is associated with the disease process of CD. The purpose of this study was to investigate the contribution of MAT to intestinal fibrosis. Methods MAT from surgical specimens of fibrostenotic CD patients and controls was collected for measurement of the levels of autotaxin [ATX] and lysophosphatidic acid [LPA]. ATX was inhibited in vivo in DNBS [dinitrobenzene sulfonic acid]-induced colitis mice, which were evaluated for colonic inflammation and fibrosis. 3T3-L1 cells and primary colonic fibroblasts were used in vitro to investigate the interaction between MAT and intestinal fibrosis, as well as the molecular mechanism underlying this interaction. Results MAT adjacent to the fibrostenotic intestine in CD patients showed an activated ATX-LPA axis. An in vivo study indicated that inhibition of ATX was associated with the improvement of morphology and function of diseased MAT, which was combined with ameliorated intestinal inflammation and fibrosis in DNBS-instilled mice. In vitro studies showed that hypoxia stimulated adipocyte ATX expression and that LPA stabilized adipocyte HIF-1 alpha protein, forming an ATX-LPA-HIF-1 alpha amplification loop and aggravating adipocyte dysfunction. LPA secreted by adipocytes bound to LPA(1) on the surface of fibroblasts, promoted their proliferation and differentiation, and increased the expression of fibrosis-related factors. Conclusions The ATX-LPA axis regulated intestinal fibrosis by influencing the proliferation and differentiation of intestinal fibroblasts. Inhibiting this axis may be a therapeutic target for intestinal fibrosis in CD.},
	keywords = {Lysophosphatidic acid; AUTOTAXIN; intestinal fibrosis; Mesenteric adipose tissue},
	year = {2022},
	eissn = {1876-4479}
}

@article{MTMT:33008120,
	title = {Preclinical detection of lysophosphatidic acid: A new window for ovarian cancer diagnostics},
	url = {https://m2.mtmt.hu/api/publication/33008120},
	author = {Huang, Xueyan and Feng, Bin and Liu, Meihui and Liu, Zuyuan and Li, Shi and Zeng, Wenbin},
	doi = {10.1016/j.talanta.2022.123561},
	journal-iso = {TALANTA},
	journal = {TALANTA},
	volume = {247},
	unique-id = {33008120},
	issn = {0039-9140},
	abstract = {Ovarian cancer, a highly metastatic disease characterized by widespread peritoneal and ascites dissemination, is the leading cause of death from gynecological malignancies and poses a serious threat to women's lives. Biomarkers detection for the early diagnosis is crucial to ameliorate the dismal survival rate. Currently, there is much interest in lysophosphatidic acid (LPA), with evidences shown that the elevated LPA level in plasma could serve as an effective biomarker for ovarian cancer. Thus the mastery of LPA measurement techniques is conducive to providing a new diagnostic or prognostic platform for ovarian cancer. In this tutorial review, with a brief discussion on the sample pre-treatment protocols, we summarize various methods for LPA detection with emphasis on the advances in universal mass spectrometry-based technologies and emerging optical sensor strategies. Meanwhile, other methods such as enzymatic method, capillary electrophoresis, dot immunogold filtration assay and bioassay are also included. Eventually, we outlook the potential clinical value of LPA detection, and anticipate the future improvements of these methodologies to make them truly useful for ovarian cancer diagnosis.},
	keywords = {biomarker; Ovarian cancer; Lysophosphatidic acid; optical sensor; mass spectroscopy},
	year = {2022},
	eissn = {1873-3573}
}

@article{MTMT:33008108,
	title = {LPA suppresses T cell function by altering the cytoskeleton and disrupting immune synapse formation},
	url = {https://m2.mtmt.hu/api/publication/33008108},
	author = {Kremer, Kimberly N. and Buser, Alan and Thumkeo, Dean and Narumiya, Shuh and Jacobelli, Jordan and Pelanda, Roberta and Torres, Raul M.},
	doi = {10.1073/pnas.2118816119},
	journal-iso = {P NATL ACAD SCI USA},
	journal = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
	volume = {119},
	unique-id = {33008108},
	issn = {0027-8424},
	abstract = {Cancer and chronic infections often increase levels of the bioactive lipid, lysophosphatitarget cell formation, IP3R1 localizes to the IS by a process dependent on mDia1 and actin and microtubule polymerization. LPA not only inhibited IP3R1 from reaching the IS but also altered T cell receptor (TCR)-induced localization of RhoA and mDia1 impairing F-actin accumulation and altering the tubulin code. Consequently, LPA impeded calcium store release and IS-directed cytokine secretion. Thus, targeting LPA signaling in chronic inflammatory conditions may rescue T cell function and promote antiviral and antitumor immunity.},
	keywords = {CYTOSKELETON; TCR; LPA; Immune Synapse},
	year = {2022},
	eissn = {1091-6490}
}

@article{MTMT:33184467,
	title = {Compensatory Upregulation of LPA(2) and Activation of the PI3K-Akt Pathway Prevent LPA(5)-Dependent Loss of Intestinal Epithelial Cells in Intestinal Organoids},
	url = {https://m2.mtmt.hu/api/publication/33184467},
	author = {Liang, Zhongxing and Yun, C. Chris},
	doi = {10.3390/cells11142243},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {11},
	unique-id = {33184467},
	abstract = {Renewal of the intestinal epithelium is orchestrated by regenerative epithelial proliferation within crypts. Recent studies have shown that lysophosphatidic acid (LPA) can maintain intestinal epithelial renewal in vitro and conditional deletion of Lpar5 (Lpar5(iKO)) in mice ablates the intestinal epithelium and increases morbidity. In contrast, constitutive Lpar5 deletion (Lpar5(cKO)) does not cause a defect in intestinal crypt regeneration. In this study, we investigated whether another LPA receptor (LPAR) compensates for constitutive loss of LPA(5) function to allow regeneration of intestinal epithelium. In Lpar5(cKO) intestinal epithelial cells (IECs), Lpar2 was upregulated and blocking LPA(2) function reduced proliferation and increased apoptosis of Lpar5(cKO) IECs. Similar to Lpar5(cKO) mice, the absence of Lpar2 (Lpar2(-/-)) resulted in upregulation of Lpar5 in IECs, indicating that LPA(2) and LPA(5) reciprocally compensate for the loss of each other. Blocking LPA(2) in Lpar5(cKO) enteroids reduced phosphorylation of Akt, indicating that LPA(2) maintains the growth of Lpar5(cKO) enteroids through activation of the PI3K-Akt pathway. The present study provides evidence that loss of an LPAR can be compensated by another LPAR. This ability to compensate needs to be considered in studies aimed to define receptor functions or test the efficacy of a LPAR-targeting drug using genetically engineered animal models.},
	keywords = {INTESTINE; Epithelial Cells; Lysophosphatidic acid; Organoid; LPA5},
	year = {2022},
	eissn = {2073-4409}
}

@article{MTMT:33328981,
	title = {Concise Synthesis of Glycerophospholipids},
	url = {https://m2.mtmt.hu/api/publication/33328981},
	author = {Mukhopadhyay, Tufan K. and Trauner, Dirk},
	doi = {10.1021/acs.joc.2c02096},
	journal-iso = {J ORG CHEM},
	journal = {JOURNAL OF ORGANIC CHEMISTRY},
	unique-id = {33328981},
	issn = {0022-3263},
	abstract = {Glycerophospholipids are major components of cellular membranes and provide important signaling molecules. Besides shaping membrane properties, some bind to specific receptors to activate biological pathways. Untangling the roles of individual glycerophospholipids requires clearly defined molecular species, a challenge that can be best addressed through chemical synthesis. However, glycerophospholipid syntheses are often lengthy due to the contrasting polarities found within these lipids. We now report a general strategy to quickly access glycerophos-pholipids via opening of a phosphate triester epoxide with carboxylic acids catalyzed by Jacobsen's Co(salen) complex. We show that this method can be applied to a variety of commercially available fatty acids, photoswitchable fatty acids, and other carboxylic acids to provide the corresponding glycerophosphate derivatives.},
	year = {2022},
	eissn = {1520-6904}
}

@article{MTMT:33008119,
	title = {Lysophosphatidic Acid Signaling and microRNAs: New Roles in Various Cancers},
	url = {https://m2.mtmt.hu/api/publication/33008119},
	author = {Rafiyan, Mahdi and Abadi, Mohammad Hassan Jafari Najaf and Zadeh, Seyed Saeed Tamehri and Hamblin, Michael R. and Mousavi, Mahboubeh and Mirzaei, Hamed},
	doi = {10.3389/fonc.2022.917471},
	journal-iso = {FRONT ONCOL},
	journal = {FRONTIERS IN ONCOLOGY},
	volume = {12},
	unique-id = {33008119},
	abstract = {A wide range of microRNAs (miRNAs) are coded for in the human genome and contribute to the regulation of gene expression. MiRNAs are able to degrade mRNAs and/or prevent the RNA transcript from being translated through complementary binding of the miRNA seed region (nucleotide 2-8) to the 3'-untranslated regions of many mRNAs. Although miRNAs are involved in almost all processes of normal human cells, they are also involved in the abnormal functions of cancer cells. MiRNAs can play dual regulatory roles in cancer, acting either as tumor suppressors or as tumor promoters, depending on the target, tumor type, and stage. In the current review, we discuss the present status of miRNA modulation in the setting of lysophosphatidic acid (LPA) signaling. LPA is produced from lysophosphatidylcholine by the enzyme autotaxin and signals via a range of G protein-coupled receptors to affect cellular processes, which ultimately causes changes in cell morphology, survival, proliferation, differentiation, migration, and adhesion. Several studies have identified miRNAs that are over-expressed in response to stimulation by LPA, but their functional roles have not yet been fully clarified. Since RNA-based treatments hold tremendous promise in the area of personalized medicne, many efforts have been made to bring miRNAs into clinical trials, and this field is evolving at an increasing pace.},
	keywords = {CANCER; MOLECULAR MECHANISM; microRNA; Lysophosphatidic acid; lysophosphatidic acid receptor},
	year = {2022},
	eissn = {2234-943X}
}

@article{MTMT:33008123,
	title = {Structure-based discovery of (S)-2-amino-6-(4-fluorobenzyl)-5,6,11,11a-tetrahydro-1H-imidazo[1 ',5 ':1,6]pyrido[3,4-b]indole-1,3(2H)-dione as low nanomolar, orally bioavailable autotaxin inhibitor},
	url = {https://m2.mtmt.hu/api/publication/33008123},
	author = {Roy, Ashis and Sarkar, Tonmoy and Datta, Sebak and Maiti, Arup and Chakrabarti, Monali and Mondal, Trisha and Mondal, Chaitali and Banerjee, Apurba and Roy, Subhasis and Mukherjee, Soumen and Muley, Pragati and Chakraborty, Sabyasachi and Banerjee, Manish and Kundu, Mrinalkanti and Roy, Kuldeep K.},
	doi = {10.1111/cbdd.14017},
	journal-iso = {CHEM BIOL DRUG DES},
	journal = {CHEMICAL BIOLOGY & DRUG DESIGN},
	volume = {99},
	unique-id = {33008123},
	issn = {1747-0277},
	abstract = {Inhibition of extracellular secreted enzyme autotaxin (ATX) represents an attractive strategy for the development of new therapeutics to treat various diseases and a few inhibitors entered in clinical trials. We herein describe structure-based design, synthesis, and biological investigations revealing a potent and orally bioavailable ATX inhibitor 1. During the molecular docking and scoring studies within the ATX enzyme (PDB-ID: 4ZGA), the S-enantiomer (Gscore = -13.168 kcal/mol) of the bound ligand PAT-494 scored better than its R-enantiomer (Gscore = -9.562 kcal/mol) which corroborated with the reported observation and analysis of the results suggested the scope of manipulation of the hydantoin substructure in PAT-494. Accordingly, the docking-based screening of a focused library of 10 compounds resulted in compound 1 as a better candidate for pharmacological studies. Compound 1 was synthesized from L-tryptophan and evaluated against ATX enzymatic activities with an IC50 of 7.6 and 24.6 nM in biochemical and functional assays, respectively. Further, ADME-PK studies divulged compound 1 as non-cytotoxic (19.02% cell growth inhibition at 20 mu M in human embryonic kidney cells), metabolically stable against human liver microsomes (CLint = 15.6 mu l/min/mg; T-1/2 = 113.2 min) with solubility of 4.82 mu M and orally bioavailable, demonstrating its potential to be used for in vivo experiments.},
	keywords = {In Vitro; DRUG DESIGN; Docking; ADME; pK; AUTOTAXIN; aminohydantoin},
	year = {2022},
	eissn = {1747-0285},
	pages = {496-503}
}

@article{MTMT:32373218,
	title = {2-Carba-lysophosphatidic acid is a novel beta-lysophosphatidic acid analogue with high potential for lysophosphatidic acid receptor activation and autotaxin inhibition},
	url = {https://m2.mtmt.hu/api/publication/32373218},
	author = {Fukasawa, Keiko and Gotoh, Mari and Uwamizu, Akiharu and Hirokawa, Takatsugu and Ishikawa, Masaki and Shimizu, Yoshibumi and Yamamoto, Shinji and Iwasa, Kensuke and Yoshikawa, Keisuke and Aoki, Junken and Murakami-Murofushi, Kimiko},
	doi = {10.1038/s41598-021-96931-2},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32373218},
	abstract = {Cyclic phosphatidic acid (cPA) is a naturally occurring phospholipid mediator that, along with its chemically stabilized analogue 2-carba-cyclic phosphatidic acid (2ccPA), induces various biological activities in vitro and in vivo. Although cPA is similar to lysophosphatidic acid (LPA) in structure and synthetic pathway, some of cPA biological functions apparently differ from those reported for LPA. We previously investigated the pharmacokinetic profile of 2ccPA, which was found to be rapidly degraded, especially in acidic conditions, yielding an unidentified compound. Thus, not only cPA but also its degradation compound may contribute to the biological activity of cPA, at least for 2ccPA. In this study, we determined the structure and examined the biological activities of 2-carba-lysophosphatidic acid (2carbaLPA) as a 2ccPA degradation compound, which is a type of beta-LPA analogue. Similar to LPA and cPA, 2carbaLPA induced the phosphorylation of the extracellular signal-regulated kinase and showed potent agonism for all known LPA receptors (LPA(1-6)) in the transforming growth factor-alpha (TGF alpha) shedding assay, in particular for LPA(3) and LPA(4). 2carbaLPA inhibited the lysophospholipase D activity of autotaxin (ATX) in vitro similar to other cPA analogues, such as 2ccPA, 3-carba-cPA, and 3-carba-LPA (alpha-LPA analogue). Our study shows that 2carbaLPA is a novel beta-LPA analogue with high potential for the activation of some LPA receptors and ATX inhibition.},
	year = {2021},
	eissn = {2045-2322}
}

@article{MTMT:32373256,
	title = {Interfering with lysophosphatidic acid receptor edg2/lpa(1) signalling slows down disease progression in SOD1-G93A transgenic mice},
	url = {https://m2.mtmt.hu/api/publication/32373256},
	author = {Gento-Caro, Angela and Vilches-Herrando, Esther and Garcia-Morales, Victoria and Portillo, Federico and Rodriguez-Bey, Guillermo and Gonzalez-Forero, David and Moreno-Lopez, Bernardo},
	doi = {10.1111/nan.12699},
	journal-iso = {NEUROPATH APPL NEURO},
	journal = {NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY},
	unique-id = {32373256},
	issn = {0305-1846},
	abstract = {Aims Alterations in excitability represent an early hallmark in Amyotrophic Lateral Sclerosis (ALS). Therefore, deciphering the factors that impact motor neuron (MN) excitability offers an opportunity to uncover further aetiopathogenic mechanisms, neuroprotective agents, therapeutic targets, and/or biomarkers in ALS. Here, we hypothesised that the lipokine lysophosphatidic acid (lpa) regulates MN excitability via the G-protein-coupled receptor lpa(1). Then, modulating lpa(1)-mediated signalling might affect disease progression in the ALS SOD1-G93A mouse model.Methods The influence of lpa-lpa(1) signalling on the electrical properties, Ca2+ dynamic and survival of MNs was tested in vitro. Expression of lpa(1) in cultured MNs and in the spinal cord of SOD1-G93A mice was analysed. ALS mice were chronically treated with a small-interfering RNA against lpa(1) (siRNA(lpa1)) or with the lpa(1) inhibitor AM095. Motor skills, MN loss, and lifespan were evaluated.Results AM095 reduced MN excitability. Conversely, exogenous lpa increased MN excitability by modulating task1 'leak' potassium channels downstream of lpa(1). Lpa-lpa(1) signalling evoked an excitotoxic response in MNs via voltage-sensitive calcium channels. Cultured SOD1-G93A MNs displayed lpa(1) upregulation and heightened vulnerability to lpa. In transgenic mice, lpa(1) was upregulated mostly in spinal cord MNs before cell loss. Chronic administration of either siRNA(lpa1) or AM095 reduced lpa(1) expression at least in MNs, delayed MN death, improved motor skills, and prolonged life expectancy of ALS mice.Conclusions These results suggest that stressed lpa-lpa(1) signalling contributes to MN degeneration in SOD1-G93A mice. Consequently, disrupting lpa(1) slows down disease progression. This highlights LPA(1) signalling as a potential target and/or biomarker in ALS.},
	keywords = {neurodegeneration; excitotoxicity; neuroprotection; amyotrophic lateral sclerosis; LPA(1); Edg2; background potassium channels; intrinsic membrane excitability; vzg1; SOD1‐; G93A model},
	year = {2021},
	eissn = {1365-2990},
	orcid-numbers = {Garcia-Morales, Victoria/0000-0002-8964-9935; Rodriguez-Bey, Guillermo/0000-0003-3597-0245; Moreno-Lopez, Bernardo/0000-0003-2897-6227}
}

@article{MTMT:32371960,
	title = {Interplay between LPA2 and LPA3 in LPA-mediated phosphatidylserine cell surface exposure and extracellular vesicles release by erythrocytes},
	url = {https://m2.mtmt.hu/api/publication/32371960},
	author = {Hasse, Stephan and Duchez, Anne-Claire and Fortin, Paul and Boilard, Eric and Bourgoin, Sylvain G.},
	doi = {10.1016/j.bcp.2021.114667},
	journal-iso = {BIOCHEMIC PHARMACOL},
	journal = {BIOCHEMICAL PHARMACOLOGY},
	volume = {192},
	unique-id = {32371960},
	issn = {0006-2952},
	abstract = {Evidence is growing for the role of red blood cells (RBCs) in vascular homeostasis, including thrombogenic events and inflammation. Lysophosphatidic acid (LPA) is known to induce phosphatidylserine (PS) exposure and the release of RBC Extracellular Vesicles (REVs). Using high sensitivity flow cytometry, we examined the effects and the mechanisms by which the LPA species commonly found in human plasma could activate RBCs. We report that LPA 16:0, 18:0 and 18:1, but not LPA 20:4, induced PS exposure and the release of small PS and large PS+ REVs through LPA3 receptor signalling in RBCs. The release of large PS+ REVs required higher concentrations of LPA. RBCs were not activated by LPA 20:4. Interestingly, blockade of LPA2 enhanced LPA-mediated PS REV release in RBCs. Furthermore, LPA receptor agonists and antagonists highlighted that LPA 20:4 inhibited LPA3dependent PS exposure and, through the LPA2 receptor, inhibited PS REV production. Activation of RBCs with LPA 18:1 in normal plasma stimulated the release of PS and PS+ REVs. REVs released in response to LPA were similar to those found in the plasma of systemic lupus erythematosus patients. Our results suggest that LPA species exhibit different biological activities in RBCs through targeting LPA2 and/or LPA3 receptors.},
	keywords = {ERYTHROCYTES; PHOSPHATIDYLSERINE; Autoimmunity; LPA; Extracellular vesicles; LPA receptors},
	year = {2021},
	eissn = {1873-2968}
}

@article{MTMT:32373254,
	title = {Increased Levels of Renal Lysophosphatidic Acid in Rodent Models with Renal Disease},
	url = {https://m2.mtmt.hu/api/publication/32373254},
	author = {Hirata, Takashi and Smith, Stanley V and Takahashi, Teisuke and Miyata, Noriyuki and Roman, Richard J.},
	doi = {10.1124/jpet.120.000353},
	journal-iso = {J PHARMACOL EXP THER},
	journal = {JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS},
	volume = {376},
	unique-id = {32373254},
	issn = {0022-3565},
	abstract = {Lysophosphatidic acid (LPA) is a bioactive lipid mediator that has been implicated in the pathophysiology of kidney disease. However, few studies have attempted to measure changes in the levels of various LPA species in the kidney after the development of renal disease. The present study measured the renal LPA levels during the development of kidney disease in rat models of hypertension, diabetes, and obstructive nephropathy using liquid chromatography/mass spectrometry/mass spectrometry. LPA levels (sum of 16:0, 18:0, 18:1, 18:2, and 20:4 LPA) were higher in the renal cortex of hypertensive Dahl salt-sensitive (Dahl S) rats fed a high-salt diet than those in normotensive rats fed a low-salt diet (296.6 +/- 22.9 vs. 196.3 +/- 8.5 nmol/g protein). LPA levels were elevated in the outer medulla of the kidney of streptozotocin-induced type 1 diabetic Dahl S rats compared with control rats (624.6 +/- 129.5 vs. 318.8 +/- 17.1 nmol/g protein). LPA levels were also higher in the renal cortex of 18-month-old, type 2 diabetic nephropathy (T2DN) rats with more severe renal injury than in 6-month-old T2DN rats (184.9 +/- 20.9 vs. 116.9 +/- 6.0 nmol/g protein). LPA levels also paralleled the progression of renal fibrosis in the renal cortex of Sprague-Dawley rats after unilateral ureteral obstruction (UUO). Administration of an LPA receptor antagonist, Ki16425, reduced the degree of renal fibrosis in UUO rats. These results suggest that the production of renal LPA increases during the development of renal injury and contributes to renal fibrosis.SIGNIFICANCE STATEMENTThe present study reveals that the lysophosphatidic acid (LPA) levels increase in the kidney in rat models of hypertension, diabetes, and obstructive nephropathy, and administration of an LPA receptor antagonist attenuates renal fibrosis. Therapeutic approaches that target the formation or actions of renal LPA might be renoprotective and have therapeutic potential.},
	year = {2021},
	eissn = {1521-0103},
	pages = {240-249}
}

@article{MTMT:32373251,
	title = {Cannabinoid CB1 and CB2 receptors differentially regulate TNF-alpha-induced apoptosis and LPA(1)-mediated pro-survival signaling in HT22 hippocampal cells},
	url = {https://m2.mtmt.hu/api/publication/32373251},
	author = {Olianas, Maria C. and Dedoni, Simona and Onali, Pierluigi},
	doi = {10.1016/j.lfs.2021.119407},
	journal-iso = {LIFE SCI},
	journal = {LIFE SCIENCES},
	volume = {276},
	unique-id = {32373251},
	issn = {0024-3205},
	abstract = {Aims: The aim of the study was to investigate the interaction between cannabinoid CB1/CB2 and lysophosphatidic acid (LPA) receptors in controlling neuronal signaling and fate.Methods: HT22 hippocampal cells were treated with different cannabinoid and LPA receptor agonists and antagonists. Western blot and immunofluorescence microscopy were used to study intracellular signaling and the expression of apoptotic markers. Cell viability was determined by a luminescence assay.Key findings: Cannabinoid agonists induced activation of both ERK1/2 and p38 MAP kinases. The effects of the CB1/CB2 receptor agonist HU210 were antagonized by the CB1 antagonist rimonabant, whereas the responses to the CB2 agonist JWH133 were blocked by the CB2 antagonist SR144528. HU210 reduced the apoptotic cell death induced by the pro-inflammatory cytokine TNF-alpha, whereas JWH133 enhanced the cytokine cytotoxicity. Blockade of ERK1/2 and p38 MAPK activation abrogated the HU210 pro-survival and the JWH133 pro-apoptotic effects, respectively. HU210 and the endocannabinoid anandamide, but not JWH133, potentiated ERK1/2 stimulation by LPA and the tricyclic antidepressant amitriptyline acting through the LPA(1) receptor. HU210 enhanced amitriptyline-stimulated CREB phosphorylation and protection against TNF-alpha-induced apoptosis, whereas JWH133 had no effect. ERK1/2 stimulation by either HU210 or amitriptyline was dependent on fibroblast growth factor receptor (FGF-R) kinase activity and the combination of the two stimulants induced FGFR phosphorylation. Moreover, the CB1 receptor was found to co-immunoprecipitate with the LPA(1) receptor.Conclusions: In HT22 hippocampal cells CB1 and CB2 receptors differentially regulate TNF-alpha-induced apoptosis and CB1 receptors positively interact with amitriptyline-stimulated LPA(1) in promoting FGF-R-mediated ERK1/2 signaling and neuroprotection.},
	keywords = {APOPTOSIS; Cannabinoid receptors; Tumor necrosis factor-alpha; amitriptyline; MAP kinases; HT22 hippocampal cells; Lysophosphatidic acid 1 receptor},
	year = {2021},
	eissn = {1879-0631}
}

@article{MTMT:32373252,
	title = {Lysophosphatidic acid (LPA)-antibody (504B3) engagement detected by interferometry identifies off-target binding},
	url = {https://m2.mtmt.hu/api/publication/32373252},
	author = {Ray, Manisha and Kihara, Yasuyuki and Bornhop, Darryl J. and Chun, Jerold},
	doi = {10.1186/s12944-021-01454-4},
	journal-iso = {LIPIDS HEALTH DIS},
	journal = {LIPIDS IN HEALTH AND DISEASE},
	volume = {20},
	unique-id = {32373252},
	issn = {1476-511X},
	abstract = {Background Lysophosphatidic acid (LPA) is a bioactive lysophospholipid that acts through its six cognate G protein-coupled receptors. As a family, lysophospholipids have already produced medicines (e.g., sphingosine 1-phosphate) as is being pursued for LPA through the use of specific antibodies that reduce ligand availability. Methods The binding properties of a commercially available, reportedly specific, monoclonal LPA antibody named 504B3 that is related to the clinical candidate Lpathomab/LT3015 were reexamined using a free solution assay (FSA) measured in a compensated interferometric reader (CIR). Results Measurement of 504B3 binding properties with an FSA-CIR approach revealed similar binding affinities for 504B3 against LPA as well as the non-LPA lipids, phosphatidic acid (PA) and lysophosphatidylcholine (LPC). Conclusions Antibody binding specificity and sensitivity, particularly involving lipid ligands, can be assessed in solution and without labels using FSA-CIR. These findings could affect interpretations of both current and past basic and clinical studies employing 504B3 and related anti-LPA antibodies.},
	keywords = {ANTIBODY; ligand binding; Lysophosphatidic acid; lysophospholipid; compensated interferometric reader; Lpathomab},
	year = {2021},
	eissn = {1476-511X}
}

@article{MTMT:32373253,
	title = {Enhancement of Cornified Envelope-Related Gene and Protein Expression by Carba Cyclic Phosphatidic Acid in Normal Human Epidermal Keratinocytes},
	url = {https://m2.mtmt.hu/api/publication/32373253},
	author = {Saito, Erika and Kage, Madoka and Tokudome, Yoshihiro},
	doi = {10.1248/bpb.b20-00572},
	journal-iso = {BIOL PHARM BULL},
	journal = {BIOLOGICAL & PHARMACEUTICAL BULLETIN},
	volume = {44},
	unique-id = {32373253},
	issn = {0918-6158},
	abstract = {The aim of this study was to examine the effects of carba cyclic phosphatidic acid (ccPA) on cornified envelope (CE) formation and keratinocyte differentiation. ccPA-treated keratinocytes showed higher mRNA and protein levels of differentiation markers and CE components than untreated cells. These results suggest that ccPA could serve as therapeutic targets for treating skin barrier dysfunction because of their roles in upregulating genes and proteins associated with CE formation and keratinocyte differentiation.},
	keywords = {skin barrier; Keratinocyte differentiation; cyclic phosphatidic acid; cornified envelope},
	year = {2021},
	eissn = {1347-5215},
	pages = {453-457}
}

@article{MTMT:32371959,
	title = {Altered plasma levels of lysophospholipids in response to adrenalectomy of rats},
	url = {https://m2.mtmt.hu/api/publication/32371959},
	author = {Tsutsumi, Toshihiko and Ino, Masaki and Shimizu, Yoshibumi and Kawabata, Kohei and Nishi, Hiroyuki and Tokumura, Akira},
	doi = {10.1016/j.prostaglins.2021.106579},
	journal-iso = {PROSTAG OTH LIPID M},
	journal = {PROSTAGLANDINS & OTHER LIPID MEDIATORS},
	volume = {156},
	unique-id = {32371959},
	issn = {1098-8823},
	abstract = {The aim of this study was to investigate effects of reduced stress hormone by adrenalectomy on rat plasma levels of lysophosphatidic acid (LPA) and other lysophospholipids. We measured activities of lysophospholipase D (lysoPLD) in plasma and lipid phosphate phosphatase (LPP) in blood by determining choline and inorganic phosphate, respectively. LPA, lysophosphatidylcholine (LPC), lysophosphatidylethanolamine (LPE), lysophosphatidylinositol (LPI), lysophosphatidylserine (LPS) and lysophosphatodylglycerol were quantified by LC-MS/ MS. In adrenalectomized rats, plasma levels of LPA, LPE, LPS and LPI, but not LPC, were increased. The increased level of LPA were due to decreased LPC level, increases plasma activity of lysoPLD toward LPC and decreased LPP activity toward LPA. Daily injections of deoxycoricosterone into rats selectively reversed increased level of LPS. Our results suggest enzymatic mechanism for increased plasma level of LPA, and indicate that the circulating levels of lysophospholipids including LPA in rats are differently affected by artificial suppression of release of adrenergic hormones.},
	keywords = {LYSOPHOSPHATIDYLCHOLINE; lysophospholipase; Rat plasma; Lysophosphatidic acid; Liquid chromatography-tandem mass spectrometry; deoxycorticosterone; Lysophospholipase D; lipid phosphate phosphatase},
	year = {2021},
	eissn = {2212-196X}
}

@article{MTMT:32373257,
	title = {The adaptation of lipid profile of human fibroblasts to alginate 2D films and 3D printed scaffolds},
	url = {https://m2.mtmt.hu/api/publication/32373257},
	author = {Zanotti, Ilaria and Marando, Silvia and Remaggi, Giulia and Bergonzi, Carlo and Bernini, Franco and Bettini, Ruggero and Elviri, Lisa},
	doi = {10.1016/j.bbagen.2020.129734},
	journal-iso = {BBA-GEN SUBJECTS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS},
	volume = {1865},
	unique-id = {32373257},
	issn = {0304-4165},
	abstract = {Background: The investigation of the interactions between cells and active materials is pivotal in the emerging 3D printing-biomaterial application fields. Here, lipidomics has been used to explore the early impact of alginate (ALG) hydrogel architecture (2D films or 3D printed scaffolds) and the type of gelling agent (CaCl2 or FeCl3) on the lipid profile of human fibroblasts.Methods: 2D and 3D ALG scaffolds were prepared and characterized in terms of water content, swelling, mechanical resistance and morphology before human fibroblast seeding (8 days). Using a liquid chromatographytriple quadrupole-tandem mass spectrometry approach, selected ceramides (CER), lysophosphatidylcholines (LPC), lysophosphatidic acids (LPA) and free fatty acids (FFA) were analyzed.Results: The results showed a clear alteration in the CER expression profile depending of both the geometry and the gelling agent used to prepare the hydrogels. As for LPCs, the main parameter affecting their distribution is the scaffold architecture with a significant decrease in the relative expression levels of the species with higher chain length (C20 to C22) for 3D scaffolds compared to 2D films. In the case of FFAs and LPAs only slight differences were observed as a function of scaffold geometry or gelling agent.Conclusions: Variations in the cell membrane lipid profile were observed for 3D cell cultures compared to 2D and these data are consistent with activation processes occurring through the mutual interactions between fibroblasts and ALG support. These unknown physiologically relevant changes add insights into the discussion about the relationship between biomaterial and the variations of cell biological functions.},
	keywords = {fatty acids; Lysophosphatidylcholines; HUMAN FIBROBLASTS; Liquid chromatography-Mass spectrometry; Ceramides; Alginate; 3D printing; Lysophosphatidic acids},
	year = {2021},
	eissn = {1872-8006},
	orcid-numbers = {Remaggi, Giulia/0000-0001-7488-1136}
}

@article{MTMT:31688911,
	title = {Potential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients},
	url = {https://m2.mtmt.hu/api/publication/31688911},
	author = {Garcia-Marchena, Nuria and Pizarro, Nieves and Pavon, Francisco J. and Martinez-Huelamo, Miriam and Flores-Lopez, Maria and Requena-Ocana, Nerea and Araos, Pedro and Silva-Pena, Daniel and Suarez, Juan and Santin, Luis J. and de la Torre, Rafael and Rodriguez de Fonseca, Fernando and Serrano, Antonia},
	doi = {10.1038/s41598-020-74155-0},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {10},
	unique-id = {31688911},
	abstract = {Lysophosphatidic acid (LPA) species are bioactive lipids participating in neurodevelopmental processes. The aim was to investigate whether the relevant species of LPA were associated with clinical features of alcohol addiction. A total of 55 abstinent alcohol use disorder (AUD) patients were compared with 34 age/sex/body mass index-matched controls. Concentrations of total LPA and 16:0-LPA, 18:0-LPA, 18:1-LPA, 18:2-LPA and 20:4-LPA species were quantified and correlated with neuroplasticity-associated growth factors including brain derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and IGF-2, and neurotrophin-3 (NT-3). AUD patients showed dysexecutive syndrome (22.4%) and memory impairment (32.6%). Total LPA, 16:0-LPA, 18:0-LPA and 18:1-LPA concentrations, were decreased in the AUD group compared to control group. Total LPA, 16:0-LPA, 18:2-LPA and 20:4-LPA concentrations were decreased in men compared to women. Frontal lobe functions correlated with plasma LPA species. Alcohol-cognitive impairments could be related with the deregulation of the LPA species, especially in 16:0-LPA, 18:1-LPA and 20:4-LPA. Concentrations of BDNF correlated with total LPA, 18:2-LPA and 20:4-LPA species. The relation between LPA species and BDNF is interesting in plasticity and neurogenesis functions, their involvement in AUD might serve as a biomarker of cognitive impairment.},
	year = {2020},
	eissn = {2045-2322}
}

@article{MTMT:31229812,
	title = {Antidepressants induce profibrotic responses via the lysophosphatidic acid receptor LPA1},
	url = {https://m2.mtmt.hu/api/publication/31229812},
	author = {Olianas, M.C. and Dedoni, S. and Onali, P.},
	doi = {10.1016/j.ejphar.2020.172963},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {873},
	unique-id = {31229812},
	issn = {0014-2999},
	year = {2020},
	eissn = {1879-0712}
}

@article{MTMT:31249935,
	title = {1-O-alkyl glycerophosphate-induced CD36 expression drives oxidative stress in microglial cells},
	url = {https://m2.mtmt.hu/api/publication/31249935},
	author = {Tsukahara, T.},
	doi = {10.1016/j.cellsig.2019.109459},
	journal-iso = {CELL SIGNAL},
	journal = {CELLULAR SIGNALLING},
	volume = {65},
	unique-id = {31249935},
	issn = {0898-6568},
	year = {2020},
	eissn = {1873-3913}
}

@article{MTMT:31249936,
	title = {Early potential metabolic biomarkers of primary postpartum haemorrhage based on serum metabolomics},
	url = {https://m2.mtmt.hu/api/publication/31249936},
	author = {Chen, T. and Zhang, R. and Zhang, Y. and Yuan, W.},
	doi = {10.5603/GP.2019.0105},
	journal-iso = {GINEKOL POL},
	journal = {GINEKOLOGIA POLSKA},
	volume = {90},
	unique-id = {31249936},
	issn = {0017-0011},
	year = {2019},
	eissn = {2543-6767},
	pages = {607-615}
}

@article{MTMT:30515631,
	title = {Cell type-selective pathways and clinical associations of lysophosphatidic acid biosynthesis and signaling in the ovarian cancer microenvironment},
	url = {https://m2.mtmt.hu/api/publication/30515631},
	author = {Reinartz, Silke and Lieber, Sonja and Pesek, Jelena and Brandt, Dominique T. and Asafova, Alina and Finkernagel, Florian and Watzer, Bernard and Nockher, Wolfgang Andreas and Nist, Andrea and Stiewe, Thorsten and Jansen, Julia M. and Wagner, Uwe and Konzer, Anne and Graumann, Johannes and Grosse, Robert and Worzfeld, Thomas and Mueller-Bruesselbach, Sabine and Mueller, Rolf},
	doi = {10.1002/1878-0261.12396},
	journal-iso = {MOL ONCOL},
	journal = {MOLECULAR ONCOLOGY},
	volume = {13},
	unique-id = {30515631},
	issn = {1574-7891},
	abstract = {The peritoneal fluid of ovarian carcinoma patients promotes cancer cell invasion and metastatic spread with lysophosphatidic acid (LPA) as a potentially crucial mediator. However, the origin of LPA in ascites and the clinical relevance of individual LPA species have not been addressed. Here, we show that the levels of multiple acyl-LPA species are strongly elevated in ascites versus plasma and are associated with short relapse-free survival. Data derived from transcriptome and secretome analyses of primary ascite-derived cells indicate that (a) the major route of LPA synthesis is the consecutive action of a secretory phospholipase A(2) (PLA(2)) and autotaxin, (b) that the components of this pathway are coordinately upregulated in ascites, and (c) that CD163+CD206+ tumor-associated macrophages play an essential role as main producers of PLA(2)G7 and autotaxin. The latter conclusion is consistent with mass spectrometry-based metabolomic analyses of conditioned medium from ascites cells, which showed that tumor-associated macrophages, but not tumor cells, are able to produce 20:4 acyl-LPA in lipid-free medium. Furthermore, our transcriptomic data revealed that LPA receptor (LPAR) genes are expressed in a clearly cell type-selective manner: While tumor cells express predominantly LPAR1-3, macrophages and T cells also express LPAR5 and LPAR6 at high levels, pointing to cell type-selective LPA signaling pathways. RNA profiling identified cytokines linked to cell motility and migration as the most conspicuous class of LPA-induced genes in macrophages, suggesting that LPA exerts protumorigenic properties at least in part via the tumor secretome.},
	keywords = {MACROPHAGE; phospholipase; Ovarian cancer; AUTOTAXIN; Lipid signaling; lysophospholipid},
	year = {2019},
	eissn = {1878-0261},
	pages = {185-201},
	orcid-numbers = {Graumann, Johannes/0000-0002-3015-5850}
}

@article{MTMT:30610562,
	title = {Regulation of tumor cell – Microenvironment interaction by the autotaxin-lysophosphatidic acid receptor axis},
	url = {https://m2.mtmt.hu/api/publication/30610562},
	author = {Tigyi, Gabor and Yue, Junming and Norman, Derek D. and Szabó, Erzsébet and Balogh, Andrea and Balazs, Louisa and Zhao, Guannan and Lee, Sue Chin},
	doi = {10.1016/j.jbior.2018.09.008},
	journal-iso = {ADV BIOL REGUL},
	journal = {ADVANCES IN BIOLOGICAL REGULATION},
	volume = {71},
	unique-id = {30610562},
	issn = {2212-4926},
	year = {2019},
	eissn = {2212-4934},
	pages = {183-193},
	orcid-numbers = {Tigyi, Gabor/0000-0001-5371-171X; Balogh, Andrea/0000-0002-3007-0793}
}

@article{MTMT:30515629,
	title = {Lysophosphatidic Acid Receptor 1 Antagonist SAR100842 for Patients With Diffuse Cutaneous Systemic Sclerosis A Double-Blind, Randomized, Eight-Week Placebo-Controlled Study Followed by a Sixteen-Week Open-Label Extension Study},
	url = {https://m2.mtmt.hu/api/publication/30515629},
	author = {Allanore, Yannick and Distler, Oliver and Jagerschmidt, Alexandre and Illiano, Stephane and Ledein, Laetitia and Boitier, Eric and Agueusop, Inoncent and Denton, Christopher P. and Khanna, Dinesh},
	doi = {10.1002/art.40547},
	journal-iso = {ARTHRITIS RHEUMATOL},
	journal = {ARTHRITIS & RHEUMATOLOGY},
	volume = {70},
	unique-id = {30515629},
	issn = {2326-5191},
	abstract = {Objective. Preclinical studies suggest a role for lysophosphatidic acid (LPA) in the pathogenesis of systemic sclerosis (SSc). We undertook this study to assess SAR100842, a potent selective oral antagonist of the LPA(1) receptor, for safety, biomarkers, and clinical efficacy in patients with diffuse cutaneous SSc (dcSSc).},
	year = {2018},
	eissn = {2326-5205},
	pages = {1634-1643}
}

@article{MTMT:30515634,
	title = {Qualitative and quantitative comparison of cyclic phosphatidic acid and its related lipid species in rat serum using hydrophilic interaction liquid chromatography with tandem-mass spectrometry},
	url = {https://m2.mtmt.hu/api/publication/30515634},
	author = {Fukasawa, Keiko and Nakajima, Shingo and Gotoh, Mari and Tanaka, Seiya and Murofushi, Hiromu and Murakami-Murofushi, Kimiko},
	doi = {10.1016/j.chroma.2018.07.010},
	journal-iso = {J CHROMATOGR A},
	journal = {JOURNAL OF CHROMATOGRAPHY A},
	volume = {1567},
	unique-id = {30515634},
	issn = {0021-9673},
	abstract = {Cyclic phosphatidic acid (cPA) is a simple lipid containing a fatty acid attached at the sn-1 position and a cyclic phosphate ring structure at the sn-2 and sn-3 positions of the glycerol backbone. The pharmacological effects of cPA have been demonstrated in several diseases such as cancer and neuropathic pain; however, the composition of the molecular species of cPA in relative to other lipid species in biological samples is still unclear. Recently, hydrophilic interaction liquid chromatography (HILIC) has demonstrated the ability to perform lipidomic analyses of biological samples. In the present study, we developed the quantitative measurement of cPA and its related lipid species, such as lysophosphatidic acid (LPA) and lysophosphatidylcholine (LPC), in rat serum using HILIC equipped with tandem-mass spectrometry (MS/MS). The lipid analysis using HILIC-MS/MS system demonstrated high linearity and reproducibility. The modified Bligh and Dyer method using citric acid was showed high efficiency on the extraction of cPA and LPA without contamination of artificial products. In rat serum, cPA and LPC contained more saturated fatty acids such as palmitic acid and stearic acid than unsaturated fatty acids, whereas LPA and phosphatidylcholine more contained unsaturated fatty acids than saturated fatty acids. The analytical methods for measuring cPA and its related lipid species in the present study will aid the analysis of their metabolism. (C) 2018 Elsevier B.V. All rights reserved.},
	keywords = {Mass spectrometry; cyclic phosphatidic acid; HILIC},
	year = {2018},
	eissn = {1873-3778},
	pages = {177-184}
}

@article{MTMT:27337308,
	title = {2-O-Carba-oleoyl cyclic phosphatidic acid induces glial proliferation through the activation of lysophosphatidic acid receptor},
	url = {https://m2.mtmt.hu/api/publication/27337308},
	author = {Nakajima, Shingo and Gotoh, Mari and Fukasawa, Keiko and Murofushi, Hiromu and Murakami-Murofushi, Kimiko},
	doi = {10.1016/j.brainres.2017.12.031},
	journal-iso = {BRAIN RES},
	journal = {BRAIN RESEARCH},
	volume = {1681},
	unique-id = {27337308},
	issn = {0006-8993},
	year = {2018},
	eissn = {1872-6240},
	pages = {44-51}
}

@article{MTMT:27691806,
	title = {Lysophosphatidic acid enhances breast cancer cells-mediated osteoclastogenesis},
	url = {https://m2.mtmt.hu/api/publication/27691806},
	author = {Nam, Ju-Suk and Sharma, Ashish Ranjan and Lich, Thi Nguyen and Jagga, Supriya and Lee, Yeon-Hee and Sharma, Garima and Lee, Sang-Soo},
	doi = {10.4196/kjpp.2018.22.5.503},
	journal-iso = {KOREAN J PHYSIOL PHA},
	journal = {KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY},
	volume = {22},
	unique-id = {27691806},
	issn = {1226-4512},
	year = {2018},
	eissn = {2093-3827},
	pages = {503-511}
}

@article{MTMT:30515542,
	title = {Pharmacologic targeting of the ATX/LPA axis attenuates bleomycin-induced pulmonary fibrosis},
	url = {https://m2.mtmt.hu/api/publication/30515542},
	author = {Ninou, Ioanna and Kaffe, Eleanna and Mueller, Stefan and Budd, David C. and Stevenson, Christopher S. and Ullmer, Christoph and Aidinis, Vassilis},
	doi = {10.1016/j.pupt.2018.08.003},
	journal-iso = {PULM PHARMACOL THER},
	journal = {PULMONARY PHARMACOLOGY & THERAPEUTICS},
	volume = {52},
	unique-id = {30515542},
	issn = {1094-5539},
	abstract = {Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease with a dismal prognosis and a largely unknown etiology. Autotaxin (ATX) is a secreted lysophospholipase D, largely responsible for extracellular production of lysophosphatidic acid (LPA), a bioactive phospholipid. LPA has numerous effects in most cell types, signaling through at least 6 receptors (LPAR) exhibiting wide spread distribution and overlapping specificities. The ATX/LPA axis has been suggested as a therapeutic target in different chronic inflammatory and fibroproliferative disorders, including pulmonary fibrosis. In this report, we examined head-to-head the efficacy of a potent inhibitor of ATX (PF-8380), that has not been tested in pulmonary fibrosis models, and an antagonist of LPAR1 (AM095) in bleomycin (BLM)-induced pulmonary fibrosis. Both compounds abrogated the development of pulmonary fibrosis and prevented the distortion of lung architecture, exhibiting qualitative and quantitative differences in different manifestations of the modeled disease.},
	keywords = {Pulmonary Fibrosis; lysophosphatidic acid (LPA); Autotaxin (ATX); Lysophospholipase D; Lysophosphatidic acid receptor 1 (LPAR1)},
	year = {2018},
	eissn = {1522-9629},
	pages = {32-40},
	orcid-numbers = {Aidinis, Vassilis/0000-0001-9531-7729}
}

@article{MTMT:30515607,
	title = {Activity and clinical relevance of autotaxin and lysophosphatidic acid pathways in high-grade serous carcinoma},
	url = {https://m2.mtmt.hu/api/publication/30515607},
	author = {Onallah, Hadil and Catane, Liora Jacobs and Trope, Claes G. and Falkenthal, Thea E. Hetland and Reich, Reuven and Davidson, Ben},
	doi = {10.1007/s00428-018-2418-x},
	journal-iso = {VIRCHOWS ARCH},
	journal = {VIRCHOWS ARCHIV},
	volume = {473},
	unique-id = {30515607},
	issn = {0945-6317},
	abstract = {The aim of this study was to analyze the expression, biological role and clinical relevance of autotaxin (ATX), the enzyme synthetizing lysophosphatidic acid (LPA), and LPA receptors (LPAR) in high-grade serous carcinoma (HGSC). mRNA expression by qRT-PCR of LPAR1-6 was analyzed in 155 HGSC specimens (88 effusions, 67 solid lesions). ATX mRNA expression was analyzed in 97 specimens. ATX, ERK, and AKT protein expression was studied by Western blotting. LPAR2 mRNA was overexpressed in HGSC cells in effusions compared to solid lesions, with opposite findings for LPAR3 and LPAR6 mRNA and ATX protein. Higher LPAR1 levels were significantly related to longer overall survival (OS) in pre-chemotherapy effusions (p = 0.027). Conversely, higher expression of LPAR1, LPAR2, and LPAR5 in post-chemotherapy effusions was significantly associated with shorter OS (p = 0.037, p = 0.025 and p = 0.021, respectively) and progression-free survival (PFS) (p < 0.001, p = 0.007 and p < 0.001, respectively) in univariate survival analysis. LPAR1 mRNA expression was an independent prognosticator of OS in patients with pre-chemotherapy effusions and PFS in patients with post-chemotherapy effusions (p = 0.013 both). In conclusion, LPAR mRNA and ATX protein levels are anatomic site-dependent in HGSC and the former are informative of disease outcome.},
	keywords = {SURVIVAL; effusion; Lysophosphatidic acid; AUTOTAXIN; High-grade serous carcinoma},
	year = {2018},
	eissn = {1432-2307},
	pages = {463-470}
}

@article{MTMT:27593271,
	title = {Systemic blockade of LPA(1/3) lysophosphatidic acid receptors by ki16425 modulates the effects of ethanol on the brain and behavior},
	url = {https://m2.mtmt.hu/api/publication/27593271},
	author = {Sanchez-Marin, Laura and Ladron, de Guevara-Miranda David and Carmen, Manas-Padilla M and Alen, Francisco and Moreno-Fernandez, Roman D and Diaz-Navarro, Caridad and Perez-del, Palacio Jose and Garcia-Fernandez, Maria and Pedraza, Carmen and Pavon, Francisco J and Rodriguez, de Fonseca Fernando and Santin, Luis J and Serrano, Antonia and Castilla-Ortega, Estela},
	doi = {10.1016/j.neuropharm.2018.01.033},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {133},
	unique-id = {27593271},
	issn = {0028-3908},
	year = {2018},
	eissn = {1873-7064},
	pages = {189-201}
}

@article{MTMT:30515633,
	title = {The interaction of beta(2)-glycoprotein I with lysophosphatidic acid in platelet aggregation and blood clotting},
	url = {https://m2.mtmt.hu/api/publication/30515633},
	author = {Sato, Akira and Nakazawa, Keiju and Sugawara, Ayano and Yamazaki, Yoji and Ebina, Keiichi},
	doi = {10.1016/j.bbapap.2018.10.004},
	journal-iso = {BBA-PROTEINS PROTEOM},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS},
	volume = {1866},
	unique-id = {30515633},
	issn = {1570-9639},
	abstract = {beta(2)-Glycoprotein I (beta(2)-GPI) is a plasma protein that binds to oxidized low-density lipoprotein (LDL) and negatively charged substances, and inhibits platelet activation and blood coagulation. In this study, we investigated the interaction of beta(2)-GPI with a negatively charged lysophosphatidic acid (LPA) in platelet aggregation and blood clotting. Two negatively charged lysophospholipids, LPA and lysophosphatidylserine, specifically inhibited the binding of beta(2)-GPI to oxidized LDL in a concentration-dependent manner. Intrinsic tryptophan fluorescence studies demonstrated that emission intensity of beta(2)-GPI decreases in an LPA-concentration-dependent manner without a shift in wavelength maxima. LPA specifically induced the aggregation of beta(2)-GPI in phosphate-buffered saline, and in incubated plasma and serum, both of which are known to accumulate LPA by the action of lecithin-cholesterol acyltransferase and lysophospholipase D/autotaxin. beta(2)-GPI aggregated by LPA did not inhibit activated von Willebrand factor-induced aggregation, and did not prolong the activated partial thromboplastin time in blood plasma, in contrast to non-aggregated beta(2)-GPI. These results suggest that . beta(2)-GPI aggregated by the binding to LPA fails to inhibit platelet aggregation and blood clotting in contrast to nonaggregated beta(2)-GPI.},
	keywords = {Platelet Aggregation; protein aggregation; Interaction; blood clotting; Lysophosphatidic acid; beta(2) -Glycoprotein I},
	year = {2018},
	eissn = {1878-1454},
	pages = {1232-1241}
}

@article{MTMT:30415844,
	title = {Prevention and treatment of secretory diarrhea by the lysophosphatidic acid analog Rx100},
	url = {https://m2.mtmt.hu/api/publication/30415844},
	author = {Thompson, Karin E. and Ray, Ramesh M. and Alli, Shanta and Ge, Wenbo and Boler, Alyssa and McCool, W. Shannon and Meena, Avtar S. and Shukla, Pradeep K. and Rao, Radakrishna and Johnson, Leonard R. and Miller, Mark A. and Tigyi, Gabor},
	doi = {10.1177/1535370218803349},
	journal-iso = {EXP BIOL MED},
	journal = {EXPERIMENTAL BIOLOGY AND MEDICINE},
	volume = {243},
	unique-id = {30415844},
	issn = {1535-3702},
	abstract = {Diarrheal disease is a severe global health problem. It is estimated that secretory diarrhea causes 2.5 million deaths annually among children under the age of five in the developing world. A critical barrier in treating diarrheal disease is lack of easy-to-use effective treatments. While antibiotics may shorten the length and severity of diarrhea, oral rehydration remains the primary approach in managing secretory diarrhea. Existing treatments mostly depend on reconstituting medicines with water that is often contaminated which can be an unresolved problem in the developing world. Standard treatments for secretory diarrhea also include drugs that decrease intestinal motility. This approach is less than ideal because in cases where infection is the cause, this can increase the incidence of bacterial translocation and the potential for sepsis. Our goal is to develop a safe, effective, easy-to-use, and inexpensive treatment to reduce fluid loss in secretory diarrhea. We have developed Rx100, which is a metabolically stable analog of lysophosphatidic acid. We tested the hypothesis that Rx100, similarly to lysophosphatidic acid, inhibits the activation of the cystic fibrosis transmembrane regulator CI channel and also reduces barrier permeability resulting in the decrease of fluid loss in multiple etiologies of secretory diarrhea. Here we have established the bioavailability and efficacy of Rx100 in cholera toxin-induced secretory diarrhea models. We have demonstrated the feasibility of Rx100 as an effective treatment for Citrobacter rodentium infection-induced secretory diarrhea. Using both the open- and closed-loop mouse models, we have optimized the dosing regimen and time line of delivery for Rx100 via oral and parenteral delivery.},
	year = {2018},
	eissn = {1535-3699},
	pages = {1056-1065},
	orcid-numbers = {Tigyi, Gabor/0000-0001-5371-171X}
}

@article{MTMT:26581591,
	title = {Management Strategies for Liver Fibrosis},
	url = {https://m2.mtmt.hu/api/publication/26581591},
	author = {Altamirano-Barrera, Alejandra and Barranco-Fragoso, Beatriz and Mendez-Sanchez, Nahum},
	doi = {10.5604/16652681.1226814},
	journal-iso = {ANN HEPATOL},
	journal = {ANNALS OF HEPATOLOGY - OFFICIAL JOURNAL OF THE MEXICAN ASSOCIATION OF HEPATOLOGY},
	volume = {16},
	unique-id = {26581591},
	issn = {1665-2681},
	year = {2017},
	eissn = {1665-2681},
	pages = {48-56}
}

@article{MTMT:3182573,
	title = {Highly Potent Non-Carboxylic Acid Autotaxin Inhibitors Reduce Melanoma Metastasis and Chemotherapeutic Resistance of Breast Cancer Stem Cells.},
	url = {https://m2.mtmt.hu/api/publication/3182573},
	author = {Banerjee, S and Norman, DD and Lee, SC and Parrill, AL and Pham, TC and Baker, DL and Tigyi, Gabor and Miller, DD},
	doi = {10.1021/acs.jmedchem.6b01270},
	journal-iso = {J MED CHEM},
	journal = {JOURNAL OF MEDICINAL CHEMISTRY},
	volume = {60},
	unique-id = {3182573},
	issn = {0022-2623},
	abstract = {Autotaxin (ATX, aka. ENPP2) is the main source of the lipid mediator lysophosphatidic acid (LPA) in biological fluids. This study reports on inhibitors of ATX derived by lead optimization of the benzene-sulfonamide in silico hit compound 3. The new analogues provide a comprehensive SAR of the benzene-sulfonamide scaffold that yielded a series of highly potent ATX inhibitors. The three most potent analogues (3a, IC50 ~ 32 nM and 3b, IC50 ~ 9 nM as well as 14, IC50 ~ 35 nM) inhibit ATX-dependent invasion of A2058 human melanoma cells in vitro. Two of the most potent compounds, 3b and 3f (IC50 ~ 84 nM) lack inhibitory action on ENPP6 and ENPP7 but possess weak antagonist action specific to the LPA1 GPCR. In particular, compound 3b potently reduced in vitro chemotherapeutic resistance of 4T1 breast cancer stem-like cells to paclitaxel and reduced significantly B16 melanoma metastasis in vivo.},
	year = {2017},
	eissn = {1520-4804},
	pages = {1309-1324},
	orcid-numbers = {Tigyi, Gabor/0000-0001-5371-171X}
}

@article{MTMT:3165272,
	title = {LPA1 receptor-mediated thromboxane A2 release is responsible for lysophosphatidic acid-induced vascular smooth muscle contraction},
	url = {https://m2.mtmt.hu/api/publication/3165272},
	author = {Dancs, Péter and Ruisanchez, Éva and Balogh, Andrea and Panta, Cecília Rita and Miklós, Zsuzsanna and Nusing, RM and Aoki, J and Chun, J and Offermanns, S and Tigyi, Gabor and Benyó, Zoltán},
	doi = {10.1096/fj.201600735R},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {31},
	unique-id = {3165272},
	issn = {0892-6638},
	abstract = {Lysophosphatidic acid (LPA) has been recognized recently as an endothelium-dependent vasodilator, but several lines of evidence indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregulation and remodeling. In the present study, mRNA expression of all 6 LPA receptor genes was detected in murine aortic VSMCs, with the highest levels of LPA1, LPA2, LPA4, and LPA6 In endothelium-denuded thoracic aorta (TA) and abdominal aorta (AA) segments, 1-oleoyl-LPA and the LPA1-3 agonist VPC31143 induced dose-dependent vasoconstriction. VPC31143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, and genetic deletion of LPA1 but not that of LPA2 or inhibition of LPA3 by diacylglycerol pyrophosphate. Surprisingly, vasoconstriction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO). VPC31143 increased thromboxane A2 (TXA2) release from TA of wild-type, TP KO, and LPA2 KO mice but not from LPA1 KO or COX1 KO mice, and PTX blocked this effect. Our findings indicate that LPA causes vasoconstriction in VSMCs, mediated by LPA1-, Gi-, and COX1-dependent autocrine/paracrine TXA2 release and consequent TP activation. We propose that this new-found interaction between the LPA/LPA1 and TXA2/TP pathways plays significant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling.-Dancs, P. T., Ruisanchez, E., Balogh, A., Panta, C. R., Miklos, Z., Nusing, R. M., Aoki, J., Chun, J., Offermanns, S., Tigyi, G., Benyo, Z. LPA1 receptor-mediated thromboxane A2 release is responsible for lysophosphatidic acid-induced vascular smooth muscle contraction.},
	year = {2017},
	eissn = {1530-6860},
	pages = {1547-1555},
	orcid-numbers = {Dancs, Péter/0000-0002-5396-5565; Ruisanchez, Éva/0000-0001-7779-226X; Balogh, Andrea/0000-0002-3007-0793; Panta, Cecília Rita/0000-0003-4162-0882; Miklós, Zsuzsanna/0000-0001-8577-4475; Tigyi, Gabor/0000-0001-5371-171X; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:26582084,
	title = {Lysophosphatidic Acid Triggers Apoptosis in HeLa Cells through the Upregulation of Tumor Necrosis Factor Receptor Superfamily Member 21},
	url = {https://m2.mtmt.hu/api/publication/26582084},
	author = {Dong, Yunzhou and Wu, Yong and Cui, Mei-Zhen and Xu, Xuemin},
	doi = {10.1155/2017/2754756},
	journal-iso = {MEDIAT INFLAMM},
	journal = {MEDIATORS OF INFLAMMATION},
	unique-id = {26582084},
	issn = {0962-9351},
	year = {2017},
	eissn = {1466-1861}
}

@article{MTMT:26724223,
	title = {Autotaxin-lysophosphatidic acid receptor signalling regulates hepatitis C virus replication},
	url = {https://m2.mtmt.hu/api/publication/26724223},
	author = {Farquhar, Michelle J and Humphreys, Isla S and Rudge, Simon A and Wilson, Garrick K and Bhattacharya, Bishnupriya and Ciaccia, Maria and Hu, Ke and Zhang, Qifeng and Mailly, Laurent and Reynolds, Gary M and Ashcroft, Margaret and Balfe, Peter and Baumert, Thomas F and Roessler, Stephanie and Wakelam, Michael J O and McKeating, Jane A},
	doi = {10.1016/j.jhep.2017.01.009},
	journal-iso = {J HEPATOL},
	journal = {JOURNAL OF HEPATOLOGY},
	volume = {66},
	unique-id = {26724223},
	issn = {0168-8278},
	year = {2017},
	eissn = {1600-0641},
	pages = {919-929},
	orcid-numbers = {Mailly, Laurent/0000-0001-6957-7463}
}

@article{MTMT:26869846,
	title = {GPCRs: Emerging anti-cancer drug targets},
	url = {https://m2.mtmt.hu/api/publication/26869846},
	author = {Gutierrez, Ainhoa Nieto and McDonald, Patricia H},
	doi = {10.1016/j.cellsig.2017.09.005},
	journal-iso = {CELL SIGNAL},
	journal = {CELLULAR SIGNALLING},
	volume = {41},
	unique-id = {26869846},
	issn = {0898-6568},
	abstract = {G protein-coupled receptors (GPCRs) constitute the largest and most diverse protein family in the human genome with over 800 members identified to date. They play critical roles in numerous cellular and physiological processes, including cell proliferation, differentiation, neurotransmission, development and apoptosis. Consequently, aberrant receptor activity has been demonstrated in numerous disorders/diseases, and as a result GPCRs have become the most successful drug target class in pharmaceuticals treating a wide variety of indications such as pain, inflammation, neurobiological and metabolic disorders. Many independent studies have also demonstrated a key role for GPCRs in tumourigenesis, establishing their involvement in cancer initiation, progression, and metastasis. Given the growing appreciation of the role(s) that GPCRs play in cancer pathogenesis, it is surprising to note that very few GPCRs have been effectively exploited in pursuit of anti-cancer therapies. The present review provides a broad overview of the roles that various GPCRs play in cancer growth and development, highlighting the potential of pharmacologically modulating these receptors for the development of novel anti-cancer therapeutics. © 2017 Elsevier Inc.},
	keywords = {Animals; Inflammation; Humans; APOPTOSIS; metabolism; MICE; CANCER; GENETICS; DISEASE PROGRESSION; AGONISTS; PAIN; DRUG TARGETS; MOUSE; METASTASIS; review; human; animal; Cell Differentiation; gene expression regulation; priority journal; nonhuman; cell proliferation; neurotransmission; Gene Expression Regulation, Neoplastic; PROTEIN FUNCTION; drug efficacy; disease exacerbation; protein expression; antineoplastic agent; antineoplastic agent; Neoplasms; protein targeting; neoplasm; Antineoplastic Agents; cancer growth; ANTINEOPLASTIC ACTIVITY; DRUG DISCOVERY; DRUG DISCOVERY; Signalling; cabergoline; CARCINOGENESIS; drug development; G protein coupled receptor; G protein coupled receptor; protein tyrosine kinase; chemokine receptor; raloxifene; metabolic disorder; Receptors, G-Protein-Coupled; plerixafor; angiopeptin; Molecular targeted therapy; molecularly targeted therapy; GPCR; proteinase activated receptor; prostaglandin E receptor 2; Smoothened protein; LYSOPHOSPHOLIPID RECEPTOR; hippo signaling; brigatinib; degarelix; frizzled protein; mogamulizumab; sonidegib; vismodegib},
	year = {2017},
	eissn = {1873-3913},
	pages = {65-74}
}

@article{MTMT:26767372,
	title = {Preparation of functional human lysophosphatidic acid receptor 2 using a P9*expression system and an amphipathic polymer and investigation of its in vitro binding preference to G(alpha) proteins},
	url = {https://m2.mtmt.hu/api/publication/26767372},
	author = {Han, Seong-Gu and Baek, Seung-Il and Son, Tae Jin and Lee, Hyeongjin and Kim, Nam Hyuk and Yu, Yeon Gyu},
	doi = {10.1016/j.bbrc.2017.04.025},
	journal-iso = {BIOCHEM BIOPH RES CO},
	journal = {BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS},
	volume = {487},
	unique-id = {26767372},
	issn = {0006-291X},
	year = {2017},
	eissn = {1090-2104},
	pages = {103-108}
}

@article{MTMT:26767407,
	title = {Lysophosphatidic acid-induced itch is mediated by signalling of LPA(5) receptor, phospholipase D and TRPA1/TRPV1},
	url = {https://m2.mtmt.hu/api/publication/26767407},
	author = {Kittaka, Hiroki and Uchida, Kunitoshi and Fukuta, Naomi and Tominaga, Makoto},
	doi = {10.1113/JP273961},
	journal-iso = {J PHYSIOL-LONDON},
	journal = {JOURNAL OF PHYSIOLOGY-LONDON},
	volume = {595},
	unique-id = {26767407},
	issn = {0022-3751},
	year = {2017},
	eissn = {1469-7793},
	pages = {2681-2698}
}

@article{MTMT:26767371,
	title = {Blocking lysophosphatidic acid receptor 1 signaling inhibits diabetic nephropathy in db/db mice},
	url = {https://m2.mtmt.hu/api/publication/26767371},
	author = {Li, Hui Ying and Oh, Yoon Sin and Choi, Ji-Woong and Jung, Ji Yong and Jun, Hee-Sook},
	doi = {10.1016/j.kint.2016.11.010},
	journal-iso = {KIDNEY INT},
	journal = {KIDNEY INTERNATIONAL},
	volume = {91},
	unique-id = {26767371},
	issn = {0085-2538},
	year = {2017},
	eissn = {1523-1755},
	pages = {1362-1373}
}

@article{MTMT:26790146,
	title = {Lysophosphatidic acid plasma concentrations in healthy subjects: Circadian rhythm and associations with demographic, anthropometric and biochemical parameters},
	url = {https://m2.mtmt.hu/api/publication/26790146},
	author = {Michalczyk, A and Budkowska, M and Dołȩgowska, B and Chlubek, D and Safranow, K},
	doi = {10.1186/s12944-017-0536-0},
	journal-iso = {LIPIDS HEALTH DIS},
	journal = {LIPIDS IN HEALTH AND DISEASE},
	volume = {16},
	unique-id = {26790146},
	issn = {1476-511X},
	year = {2017},
	eissn = {1476-511X}
}

@article{MTMT:26424824,
	title = {Signaling via G proteins mediates tumorigenic effects of GPR87},
	url = {https://m2.mtmt.hu/api/publication/26424824},
	author = {Niss, Arfelt K and Fares, S and Sparre-Ulrich, AH and Hjortø, GM and Gasbjerg, LS and Mølleskov-Jensen, A-S and Benned-Jensen, T and Rosenkilde, MM},
	doi = {10.1016/j.cellsig.2016.11.009},
	journal-iso = {CELL SIGNAL},
	journal = {CELLULAR SIGNALLING},
	volume = {30},
	unique-id = {26424824},
	issn = {0898-6568},
	year = {2017},
	eissn = {1873-3913},
	pages = {9-18}
}

@article{MTMT:27099024,
	title = {Role of lysophosphatidic acid and its receptors in the kidney},
	url = {https://m2.mtmt.hu/api/publication/27099024},
	author = {Park, Frank and Miller, Duane D},
	doi = {10.1152/physiolgenomics.00070.2017},
	journal-iso = {PHYSIOL GENOMICS},
	journal = {PHYSIOLOGICAL GENOMICS},
	volume = {49},
	unique-id = {27099024},
	issn = {1094-8341},
	year = {2017},
	eissn = {1531-2267},
	pages = {659-666}
}

@article{MTMT:26582074,
	title = {Endogenous lysophosphatidic acid (LPA(1)) receptor agonists demonstrate ligand bias between calcium and ERK signalling pathways in human lung fibroblasts},
	url = {https://m2.mtmt.hu/api/publication/26582074},
	author = {Sattikar, Afrah and Dowling, Mark R and Rosethorne, Elizabeth M},
	doi = {10.1111/bph.13671},
	journal-iso = {BR J PHARMACOL},
	journal = {BRITISH JOURNAL OF PHARMACOLOGY},
	volume = {174},
	unique-id = {26582074},
	issn = {0007-1188},
	year = {2017},
	eissn = {1476-5381},
	pages = {227-237}
}

@article{MTMT:27099044,
	title = {Lysophospholipid-Related Diseases and PPAR gamma Signaling Pathway},
	url = {https://m2.mtmt.hu/api/publication/27099044},
	author = {Tsukahara, Tamotsu and Matsuda, Yoshikazu and Haniu, Hisao},
	doi = {10.3390/ijms18122730},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {18},
	unique-id = {27099044},
	issn = {1661-6596},
	year = {2017},
	eissn = {1422-0067}
}

@article{MTMT:27098955,
	title = {Elevated plasma levels of lysophosphatidic acid and aberrant expression of lysophosphatidic acid receptors in adenomyosis},
	url = {https://m2.mtmt.hu/api/publication/27098955},
	author = {Yang, Bicheng and Wang, Liqun and Wan, Xiaoju and Li, Yunjun and Yu, Xiaohong and Qin, Yunna and Luo, Yong and Wang, Feng and Huang, Ouping},
	doi = {10.1186/s12905-017-0474-z},
	journal-iso = {BMC WOMENS HEALTH},
	journal = {BMC WOMENS HEALTH},
	volume = {17},
	unique-id = {27098955},
	issn = {1472-6874},
	year = {2017},
	eissn = {1472-6874}
}

@article{MTMT:26413645,
	title = {G Protein-Coupled Receptors in Cancer},
	url = {https://m2.mtmt.hu/api/publication/26413645},
	author = {Bar-Shavit, Rachel and Maoz, Myriam and Kancharla, Arun and Nag, Jeetendra Kumar and Agranovich, Daniel and Grisaru-Granovsky, Sorina and Uziely, Beatrice},
	doi = {10.3390/ijms17081320},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {17},
	unique-id = {26413645},
	issn = {1661-6596},
	year = {2016},
	eissn = {1422-0067}
}

@article{MTMT:26418121,
	title = {Tg6F ameliorates the increase in oxidized phospholipids in the jejunum of mice fed unsaturated LysoPC or WD},
	url = {https://m2.mtmt.hu/api/publication/26418121},
	author = {Chattopadhyay, Arnab and Navab, Mohamad and Hough, Greg and Grijalva, Victor and Mukherjee, Pallavi and Fogelman, Hannah R and Hwang, Lin H and Faull, Kym F and Lusis, Aldons J and Reddy, Srinivasa T and Fogelman, Alan M},
	doi = {10.1194/jlr.M064352},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {57},
	unique-id = {26418121},
	issn = {0022-2275},
	year = {2016},
	eissn = {1539-7262},
	pages = {832-847}
}

@article{MTMT:26420298,
	title = {A novel approach for measuring sphingosine-1-phosphate and lysophosphatidic acid binding to carrier proteins using monoclonal antibodies and the Kinetic Exclusion Assay},
	url = {https://m2.mtmt.hu/api/publication/26420298},
	author = {Fleming, Jonathan K and Glass, Thomas R and Lackie, Steve J and Wojciak, Jonathan M},
	doi = {10.1194/jlr.D068866},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {57},
	unique-id = {26420298},
	issn = {0022-2275},
	year = {2016},
	eissn = {1539-7262},
	pages = {1737-1747}
}

@article{MTMT:26413642,
	title = {Role of ectonucleotide pyrophosphatase/phosphodiesterase 2 in the midline axis formation of zebrafish},
	url = {https://m2.mtmt.hu/api/publication/26413642},
	author = {Frisca, Frisca and Colquhoun, Daniel and Goldshmit, Yona and Anko, Minna-Liisa and Pebay, Alice and Kaslin, Jan},
	doi = {10.1038/srep37678},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {6},
	unique-id = {26413642},
	year = {2016},
	eissn = {2045-2322}
}

@article{MTMT:26416068,
	title = {Plant Lysophosphatidic Acids: A Rich Source for Bioactive Lysophosphatidic Acids and Their Pharmacological Applications},
	url = {https://m2.mtmt.hu/api/publication/26416068},
	author = {Lee, Byung-Hwan and Choi, Sun-Hye and Kim, Hyeon-Joong and Jung, Seok-Won and Kim, Ho-Kyoung and Nah, Seung-Yeol},
	doi = {10.1248/bpb.b15-00575},
	journal-iso = {BIOL PHARM BULL},
	journal = {BIOLOGICAL & PHARMACEUTICAL BULLETIN},
	volume = {39},
	unique-id = {26416068},
	issn = {0918-6158},
	year = {2016},
	eissn = {1347-5215},
	pages = {156-162}
}

@article{MTMT:26413648,
	title = {Cross-talk between lysophosphatidic acid receptor. 1 and tropomyosin receptor kinase A promotes lung epithelial cell migration},
	url = {https://m2.mtmt.hu/api/publication/26413648},
	author = {Nan, Ling and Wei, Jianxin and Jacko, Anastasia M and Culley, Miranda K and Zhao, Jing and Natarajan, Viswanathan and Ma, Haichun and Zhao, Yutong},
	doi = {10.1016/j.bbamcr.2015.11.012},
	journal-iso = {BBA-MOL CELL RES},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH},
	volume = {1863},
	unique-id = {26413648},
	issn = {0167-4889},
	year = {2016},
	eissn = {1879-2596},
	pages = {229-235}
}

@article{MTMT:26413644,
	title = {Distinct 1-monoacylglycerol and 2-monoacylglycerol kinase activities of diacylglycerol kinase isozymes},
	url = {https://m2.mtmt.hu/api/publication/26413644},
	author = {Sato, Yuriko and Murakami, Chiaki and Yamaki, Atsumi and Mizuno, Satoru and Sakai, Hiromichi and Sakane, Fumio},
	doi = {10.1016/j.bbapap.2016.06.012},
	journal-iso = {BBA-PROTEINS PROTEOM},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS},
	volume = {1864},
	unique-id = {26413644},
	issn = {1570-9639},
	year = {2016},
	eissn = {1878-1454},
	pages = {1170-1176},
	orcid-numbers = {Murakami, Chiaki/0000-0003-3645-8382; Sakane, Fumio/0000-0003-0857-0377}
}

@article{MTMT:26414545,
	title = {Differential expression of lysophosphatidic acid receptors between benign and malignant tissues in humans},
	url = {https://m2.mtmt.hu/api/publication/26414545},
	author = {Wang, Chunyi and Mao, Jinghe and Bingham, Andrew and Mo, Yingyuan and Lage, Janice and Zhou, Xinchun},
	journal-iso = {INT J CLIN EXP MED},
	journal = {INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE},
	volume = {9},
	unique-id = {26414545},
	issn = {1940-5901},
	year = {2016},
	eissn = {1940-5901},
	pages = {7952-7964}
}

@article{MTMT:26413654,
	title = {Phosphorylation and Internalization of Lysophosphatidic Acid Receptors LPA(1), LPA(2), and LPA(3)},
	url = {https://m2.mtmt.hu/api/publication/26413654},
	author = {Alcantara-Hernandez, Rocio and Hernandez-Mendez, Aurelio and Campos-Martinez, Gisselle A and Meizoso-Huesca, Aldo and Adolfo, Garcia-Sainz J},
	doi = {10.1371/journal.pone.0140583},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {10},
	unique-id = {26413654},
	year = {2015},
	eissn = {1932-6203}
}

@article{MTMT:26418709,
	title = {Lysophosphatidic Acid and Sphingosine-1-Phosphate: A Concise Review of Biological Function and Applications for Tissue Engineering},
	url = {https://m2.mtmt.hu/api/publication/26418709},
	author = {Binder, Bernard Y K and Williams, Priscilla A and Silva, Eduardo A and Leach, J Kent},
	doi = {10.1089/ten.teb.2015.0107},
	journal-iso = {TISSUE ENG PART B REV},
	journal = {TISSUE ENGINEERING PART B REVIEWS},
	volume = {21},
	unique-id = {26418709},
	issn = {1937-3368},
	year = {2015},
	eissn = {1937-3376},
	pages = {531-542}
}

@article{MTMT:26413657,
	title = {A Major Human Oral Lysophosphatidic Acid Species, LPA 18: 1, Regulates Novel Genes in Human Gingival Fibroblasts},
	url = {https://m2.mtmt.hu/api/publication/26413657},
	author = {Cerutis, D Roselyn and Weston, Michael D and Alnouti, Yazen and Bathena, Sai P and Nunn, Martha E and Ogunleye, Afolabi O and McVaney, Timothy P and Headen, Karmel V and Miyamoto, Takanari},
	doi = {10.1902/jop.2015.140592},
	journal-iso = {J PERIODONTOL},
	journal = {JOURNAL OF PERIODONTOLOGY},
	volume = {86},
	unique-id = {26413657},
	issn = {0022-3492},
	year = {2015},
	eissn = {1943-3670},
	pages = {713-725}
}

@article{MTMT:26413653,
	title = {Loss of lysophosphatidic acid receptor LPA(1) alters oligodendrocyte differentiation and myelination in the mouse cerebral cortex},
	url = {https://m2.mtmt.hu/api/publication/26413653},
	author = {Garcia-Diaz, Beatriz and Riquelme, Raquel and Varela-Nieto, Isabel and Jesus, Jimenez Antonio and de Diego, Isabel and lsabel, Gomez-Conde Ana and Matas-Rico, Elisa and Angel, Aguirre Jose and Chun, Jerold and Pedraza, Carmen and Javier, Santin Luis and Fernandez, Oscar and Rodriguez, de Fonseca Fernando and Estivill-Torrus, Guillermo},
	doi = {10.1007/s00429-014-0885-7},
	journal-iso = {BRAIN STRUCT FUNC},
	journal = {BRAIN STRUCTURE & FUNCTION},
	volume = {220},
	unique-id = {26413653},
	issn = {1863-2653},
	year = {2015},
	eissn = {1863-2661},
	pages = {3701-3720},
	orcid-numbers = {Estivill-Torrus, Guillermo/0000-0002-7124-2678}
}

@article{MTMT:26424672,
	title = {Membrane-Derived Phospholipids Control Synaptic Neurotransmission and Plasticity},
	url = {https://m2.mtmt.hu/api/publication/26424672},
	author = {Garcia-Morales, Victoria and Montero, Fernando and Gonzalez-Forero, David and Rodriguez-Bey, Guillermo and Gomez-Perez, Laura and Jesus, Medialdea-Wandossell Maria and Dominguez-Vias, German and Manuel, Garcia-Verdugo Jose and Moreno-Lopez, Bernardo},
	doi = {10.1371/journal.pbio.1002153},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {13},
	unique-id = {26424672},
	issn = {1544-9173},
	year = {2015},
	eissn = {1545-7885}
}

@article{MTMT:26414375,
	title = {Kruppel-like factor 5 incorporates into the beta-catenin/TCF complex in response to LPA in colon cancer cells},
	url = {https://m2.mtmt.hu/api/publication/26414375},
	author = {Guo, Leilei and He, Peijian and No, Yi Ran and Yun, C Chris},
	doi = {10.1016/j.cellsig.2015.02.005},
	journal-iso = {CELL SIGNAL},
	journal = {CELLULAR SIGNALLING},
	volume = {27},
	unique-id = {26414375},
	issn = {0898-6568},
	year = {2015},
	eissn = {1873-3913},
	pages = {961-968}
}

@article{MTMT:26413660,
	title = {LPA Promotes T Cell Recruitment through Synthesis of CXCL13},
	url = {https://m2.mtmt.hu/api/publication/26413660},
	author = {Hui, Weili and Zhao, Chenqi and Bourgoin, Sylvain G},
	doi = {10.1155/2015/248492},
	journal-iso = {MEDIAT INFLAMM},
	journal = {MEDIATORS OF INFLAMMATION},
	unique-id = {26413660},
	issn = {0962-9351},
	year = {2015},
	eissn = {1466-1861}
}

@article{MTMT:26413652,
	title = {Lysophosphatidic acid signaling in ovarian cancer},
	url = {https://m2.mtmt.hu/api/publication/26413652},
	author = {Jesionowska, Anna and Cecerska-Heryc, Elzbieta and Matoszka, Natalia and Dolegowska, Barbara},
	doi = {10.3109/10799893.2015.1026444},
	journal-iso = {J RECEPT SIGNAL TR},
	journal = {JOURNAL OF RECEPTOR AND SIGNAL TRANSDUCTION},
	volume = {35},
	unique-id = {26413652},
	issn = {1079-9893},
	year = {2015},
	eissn = {1532-4281},
	pages = {578-584}
}

@article{MTMT:26413655,
	title = {Biased signalling: the instinctive skill of the cell in the selection of appropriate signalling pathways},
	url = {https://m2.mtmt.hu/api/publication/26413655},
	author = {Liu, Ying and Yang, Yang and Ward, Richard and An, Su and Guo, Xiao-Xi and Li, Wei and Xu, Tian-Rui},
	doi = {10.1042/BJ20150358},
	journal-iso = {BIOCHEM J},
	journal = {BIOCHEMICAL JOURNAL},
	volume = {470},
	unique-id = {26413655},
	issn = {0264-6021},
	year = {2015},
	eissn = {1470-8728},
	pages = {155-167}
}

@article{MTMT:26417205,
	title = {Lysophosphatidic acid receptor (LPAR) modulators: The current pharmacological toolbox},
	url = {https://m2.mtmt.hu/api/publication/26417205},
	author = {Llona-Minguez, Sabin and Ghassemian, Artin and Helleday, Thomas},
	doi = {10.1016/j.plipres.2015.01.004},
	journal-iso = {PROG LIPID RES},
	journal = {PROGRESS IN LIPID RESEARCH},
	volume = {58},
	unique-id = {26417205},
	issn = {0163-7827},
	year = {2015},
	eissn = {1873-2194},
	pages = {51-75},
	orcid-numbers = {Llona-Minguez, Sabin/0000-0003-3187-722X; Helleday, Thomas/0000-0002-7384-092X}
}

@article{MTMT:26413650,
	title = {Serum Autotaxin/ENPP2 Correlates with Insulin Resistance in Older Humans with Obesity},
	url = {https://m2.mtmt.hu/api/publication/26413650},
	author = {Reeves, Valerie L and Trybula, Joy S and Wills, Rachel C and Goodpaster, Bret H and Dube, John J and Kienesberger, Petra C and Kershaw, Erin E},
	doi = {10.1002/oby.21232},
	journal-iso = {OBESITY},
	journal = {OBESITY},
	volume = {23},
	unique-id = {26413650},
	issn = {1930-7381},
	year = {2015},
	eissn = {1930-739X},
	pages = {2371-2376}
}

@article{MTMT:26413669,
	title = {Lysophosphatidic Acid Protects Human Mesenchymal Stromal Cells from Differentiation-Dependent Vulnerability to Apoptosis},
	url = {https://m2.mtmt.hu/api/publication/26413669},
	author = {Binder, Bernard Y K and Genetos, Damian C and Leach, J Kent},
	doi = {10.1089/ten.tea.2013.0487},
	journal-iso = {TISSUE ENG PT A},
	journal = {TISSUE ENGINEERING PART A},
	volume = {20},
	unique-id = {26413669},
	issn = {1937-3341},
	year = {2014},
	eissn = {1937-335X},
	pages = {1156-1164}
}

@article{MTMT:26413668,
	title = {Lysophosphatidic Acid Enhanced the Angiogenic Capability of Human Chondrocytes by Regulating Gi/NF-kappa B-Dependent Angiogenic Factor Expression},
	url = {https://m2.mtmt.hu/api/publication/26413668},
	author = {Chuang, Yi-Wen and Chang, Wen-Ming and Chen, Kai-Hua and Hong, Chang-Zern and Chang, Pey-Jium and Hsu, Hung-Chih},
	doi = {10.1371/journal.pone.0095180},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {9},
	unique-id = {26413668},
	year = {2014},
	eissn = {1932-6203}
}

@article{MTMT:26418731,
	title = {Biological Relevance of Lysophospholipids and Green Solutions for Their Synthesis},
	url = {https://m2.mtmt.hu/api/publication/26418731},
	author = {Gendaszewska-Darmach, Edyta and Drzazga, Anna},
	doi = {10.2174/1385272819666140923220851},
	journal-iso = {CURR ORG CHEM},
	journal = {CURRENT ORGANIC CHEMISTRY},
	volume = {18},
	unique-id = {26418731},
	issn = {1385-2728},
	year = {2014},
	eissn = {1875-5348},
	pages = {2928-2949}
}

@article{MTMT:2756692,
	title = {Lysophosphatidic acid receptor 5 inhibits B cell antigen receptor signaling and antibody response.},
	url = {https://m2.mtmt.hu/api/publication/2756692},
	author = {Hu, J and Oda, SK and Shotts, K and Donovan, EE and Strauch, P and Pujanauski, LM and Victorino, F and Al-Shami, A and Fujiwara, Y and Tigyi, Gabor and Oravecz, T and Pelanda, R and Torres, RM},
	doi = {10.4049/jimmunol.1300429},
	journal-iso = {J IMMUNOL},
	journal = {JOURNAL OF IMMUNOLOGY},
	volume = {193},
	unique-id = {2756692},
	issn = {0022-1767},
	abstract = {Lysophospholipids have emerged as biologically important chemoattractants capable of directing lymphocyte development, trafficking, and localization. Lysophosphatidic acid (LPA) is a major lysophospholipid found systemically, and its levels are elevated in certain pathological settings, such as cancer and infections. In this study, we demonstrate that BCR signal transduction by mature murine B cells is inhibited upon LPA engagement of the LPA5 (GPR92) receptor via a Galpha12/13-Arhgef1 pathway. The inhibition of BCR signaling by LPA5 manifests by impaired intracellular calcium store release and most likely by interfering with inositol 1,4,5-triphosphate receptor activity. We further show that LPA5 also limits Ag-specific induction of CD69 and CD86 expression and that LPA5-deficient B cells display enhanced Ab responses. Thus, these data show that LPA5 negatively regulates BCR signaling, B cell activation, and immune response. Our findings extend the influence of lysophospholipids on immune function and suggest that alterations in LPA levels likely influence adaptive humoral immunity.},
	keywords = {Animals; MICE; Mice, Knockout; B-Lymphocytes/*immunology; Signal Transduction/genetics/*immunology; Antibody Formation/*physiology; Receptors, Lysophosphatidic Acid/genetics/*immunology; Receptors, Antigen, B-Cell/genetics/*immunology; Lectins, C-Type/genetics/immunology; Immunity, Humoral/*physiology; Gene Expression Regulation/genetics/immunology; GTP-Binding Protein alpha Subunits, G12-G13/genetics/immunology; Antigens, Differentiation, T-Lymphocyte/genetics/immunology; Antigens, CD86/genetics/immunology; Antigens, CD/genetics/immunology},
	year = {2014},
	eissn = {1550-6606},
	pages = {85-95},
	orcid-numbers = {Tigyi, Gabor/0000-0001-5371-171X}
}

@article{MTMT:26413664,
	title = {Convergence of vitamin D and lysophosphatidic acid signaling in stimulating human osteoblast maturation},
	url = {https://m2.mtmt.hu/api/publication/26413664},
	author = {Mansell, J.P.},
	doi = {10.3389/fphys.2014.00263},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {5},
	unique-id = {26413664},
	year = {2014},
	eissn = {1664-042X}
}

@article{MTMT:26417950,
	title = {Docosatetraenoyl LPA is elevated in exhaled breath condensate in idiopathic pulmonary fibrosis},
	url = {https://m2.mtmt.hu/api/publication/26417950},
	author = {Montesi, Sydney B and Mathai, Susan K and Brenner, Laura N and Gorshkova, Irina A and Berdyshev, Evgeny V and Tager, Andrew M and Shea, Barry S},
	doi = {10.1186/1471-2466-14-5},
	journal-iso = {BMC PULM MED},
	journal = {BMC PULMONARY MEDICINE},
	volume = {14},
	unique-id = {26417950},
	issn = {1471-2466},
	year = {2014},
	eissn = {1471-2466}
}

@article{MTMT:26413661,
	title = {Melanoma Cells Break Down LPA to Establish Local Gradients That Drive Chemotactic Dispersal},
	url = {https://m2.mtmt.hu/api/publication/26413661},
	author = {Muinonen-Martin, Andrew J and Susanto, Olivia and Zhang, Qifeng and Smethurst, Elizabeth and Faller, William J and Veltman, Douwe M and Kalna, Gabriela and Lindsay, Colin and Bennett, Dorothy C and Sansom, Owen J and Herd, Robert and Jones, Robert and Machesky, Laura M and Wakelam, Michael J O and Knecht, David A and Insall, Robert H},
	doi = {10.1371/journal.pbio.1001966},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {12},
	unique-id = {26413661},
	issn = {1544-9173},
	year = {2014},
	eissn = {1545-7885},
	orcid-numbers = {Susanto, Olivia/0000-0001-6360-1952; Sansom, Owen J/0000-0001-9540-3010}
}

@article{MTMT:26416548,
	title = {Complexities of lysophospholipid signalling in glioblastoma},
	url = {https://m2.mtmt.hu/api/publication/26416548},
	author = {Ng, Wayne and Pebay, Alice and Drummond, Katharine and Burgess, Antony and Kaye, Andrew H and Morokoff, Andrew},
	doi = {10.1016/j.jocn.2014.02.013},
	journal-iso = {J CLIN NEUROSCI},
	journal = {JOURNAL OF CLINICAL NEUROSCIENCE},
	volume = {21},
	unique-id = {26416548},
	issn = {0967-5868},
	year = {2014},
	eissn = {1532-2653},
	pages = {893-898},
	orcid-numbers = {Pebay, Alice/0000-0002-7408-9453; Morokoff, Andrew/0000-0002-5159-3438}
}

@article{MTMT:26417473,
	title = {Challenges in accurate quantitation of lysophosphatidic acids in human biofluids},
	url = {https://m2.mtmt.hu/api/publication/26417473},
	author = {Onorato, Joelle M and Shipkova, Petia and Minnich, Anne and Aubry, Anne-Francoise and Easter, John and Tymiak, Adrienne},
	doi = {10.1194/jlr.D050070},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {55},
	unique-id = {26417473},
	issn = {0022-2275},
	year = {2014},
	eissn = {1539-7262},
	pages = {1784-1796}
}

@article{MTMT:2756690,
	title = {Design and synthesis of sulfamoyl benzoic acid analogues with subnanomolar agonist activity specific to the LPA2 receptor.},
	url = {https://m2.mtmt.hu/api/publication/2756690},
	author = {Patil, R and Fells, JI and Szabó, Erzsébet and Lim, KG and Norman, DD and Balogh, Andrea and Patil, S and Strobos, J and Miller, DD and Tigyi, Gabor},
	doi = {10.1021/jm5007116},
	journal-iso = {J MED CHEM},
	journal = {JOURNAL OF MEDICINAL CHEMISTRY},
	volume = {57},
	unique-id = {2756690},
	issn = {0022-2623},
	abstract = {Lysophosphatidic acid (LPA) is a growth factor-like mediator and a ligand for multiple GPCR. The LPA2 GPCR mediates antiapoptotic and mucosal barrier-protective effects in the gut. We synthesized sulfamoyl benzoic acid (SBA) analogues that are the first specific agonists of LPA2, some with subnanomolar activity. We developed an experimental SAR that is supported and rationalized by computational docking analysis of the SBA compounds into the LPA2 ligand-binding pocket.},
	keywords = {Humans; BINDING SITES; structure-activity relationship; DRUG DESIGN; Drug Evaluation, Preclinical/methods; Chemistry Techniques, Synthetic; Molecular Docking Simulation; Receptors, Lysophosphatidic Acid/*agonists/chemistry/metabolism; Benzoates/*chemistry},
	year = {2014},
	eissn = {1520-4804},
	pages = {7136-7140},
	orcid-numbers = {Balogh, Andrea/0000-0002-3007-0793; Tigyi, Gabor/0000-0001-5371-171X}
}

@article{MTMT:2470225,
	title = {Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase.},
	url = {https://m2.mtmt.hu/api/publication/2470225},
	author = {Ruisanchez, Éva and Dancs, Péter and Kerek, M and Nemeth, T and Faragó, Bernadett and Balogh, Andrea and Patil, R and Jennings, BL and Liliom, Károly and Malik, KU and Smrcka, AV and Tigyi, Gabor and Benyó, Zoltán},
	doi = {10.1096/fj.13-234997},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {28},
	unique-id = {2470225},
	issn = {0892-6638},
	abstract = {Lysophosphatidic acid (LPA) has been implicated as a mediator of several cardiovascular functions, but its potential involvement in the control of vascular tone is obscure. Here, we show that both LPA (18:1) and VPC31143 (a synthetic agonist of LPA1-3 receptors) relax intact mouse thoracic aorta with similar Emax values (53.9 and 51.9% of phenylephrine-induced precontraction), although the EC50 of LPA- and VPC31143-induced vasorelaxations were different (400 vs. 15 nM, respectively). Mechanical removal of the endothelium or genetic deletion of endothelial nitric oxide synthase (eNOS) not only diminished vasorelaxation by LPA or VPC31143 but converted it to vasoconstriction. Freshly isolated mouse aortic endothelial cells expressed LPA1, LPA2, LPA4 and LPA5 transcripts. The LPA1,3 antagonist Ki16425, the LPA1 antagonist AM095, and the genetic deletion of LPA1, but not that of LPA2, abolished LPA-induced vasorelaxation. Inhibition of the phosphoinositide 3 kinase-protein kinase B/Akt pathway by wortmannin or MK-2206 failed to influence the effect of LPA. However, pharmacological inhibition of phospholipase C (PLC) by U73122 or edelfosine, but not genetic deletion of PLCepsilon, abolished LPA-induced vasorelaxation and indicated that a PLC enzyme, other than PLCepsilon, mediates the response. In summary, the present study identifies LPA as an endothelium-dependent vasodilator substance acting via LPA1, PLC, and eNOS.-Ruisanchez, E., Dancs, P., Kerek, M., Nemeth, T., Farago, B., Balogh, A., Patil, R., Jennings, B. L., Liliom, K., Malik, K. U., Smrcka, A. V., Tigyi, G., Benyo, Z. Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase.},
	year = {2014},
	eissn = {1530-6860},
	pages = {880-890},
	orcid-numbers = {Ruisanchez, Éva/0000-0001-7779-226X; Dancs, Péter/0000-0002-5396-5565; Balogh, Andrea/0000-0002-3007-0793; Liliom, Károly/0000-0002-7177-6872; Tigyi, Gabor/0000-0001-5371-171X; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:26413673,
	title = {Lysophosphatidic Acid Signaling in Late Cleavage and Blastocyst Stage Bovine Embryos},
	url = {https://m2.mtmt.hu/api/publication/26413673},
	author = {Torres, Ana Catarina and Boruszewska, Dorota and Batista, Mariana and Kowalczyk-Zieba, Ilona and Diniz, Patricia and Sinderewicz, Emilia and Saulnier-Blache, Jean Sebastian and Woclawek-Potocka, Izabela and Lopes-da-Costa, Luis},
	doi = {10.1155/2014/678968},
	journal-iso = {MEDIAT INFLAMM},
	journal = {MEDIATORS OF INFLAMMATION},
	unique-id = {26413673},
	issn = {0962-9351},
	year = {2014},
	eissn = {1466-1861},
	orcid-numbers = {Diniz, Patricia/0000-0001-5303-6953}
}

@article{MTMT:26413674,
	title = {Acyltransferases and transacylases that determine the fatty acid composition of glycerolipids and the metabolism of bioactive lipid mediators in mammalian cells and model organisms},
	url = {https://m2.mtmt.hu/api/publication/26413674},
	author = {Yamashita, Atsushi and Hayashi, Yasuhiro and Nemoto-Sasaki, Yoko and Ito, Makoto and Oka, Saori and Tanikawa, Takashi and Waku, Keizo and Sugiura, Takayuki},
	doi = {10.1016/j.plipres.2013.10.001},
	journal-iso = {PROG LIPID RES},
	journal = {PROGRESS IN LIPID RESEARCH},
	volume = {53},
	unique-id = {26413674},
	issn = {0163-7827},
	year = {2014},
	eissn = {1873-2194},
	pages = {18-81}
}

@article{MTMT:24128132,
	title = {LPA receptor signaling: Pharmacology, physiology, and pathophysiology},
	url = {https://m2.mtmt.hu/api/publication/24128132},
	author = {Yung, YC and Stoddard, NC and Chun, J},
	doi = {10.1194/jlr.R046458},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {55},
	unique-id = {24128132},
	issn = {0022-2275},
	year = {2014},
	eissn = {1539-7262},
	pages = {1192-1214}
}

@article{MTMT:26414981,
	title = {Constitutive Lymphocyte Transmigration across the Basal Lamina of High Endothelial Venules Is Regulated by the Autotaxin/Lysophosphatidic Acid Axis},
	url = {https://m2.mtmt.hu/api/publication/26414981},
	author = {Bai, Zhongbin and Cai, Linjun and Umemoto, Eiji and Takeda, Akira and Tohya, Kazuo and Komai, Yutaka and Veeraveedu, Punniyakoti Thanikachalam and Hata, Erina and Sugiura, Yuki and Kubo, Akiko and Suematsu, Makoto and Hayasaka, Haruko and Okudaira, Shinichi and Aoki, Junken and Tanaka, Toshiyuki and Albers, Harald M H G and Ovaa, Huib and Miyasaka, Masayuki},
	doi = {10.4049/jimmunol.1202025},
	journal-iso = {J IMMUNOL},
	journal = {JOURNAL OF IMMUNOLOGY},
	volume = {190},
	unique-id = {26414981},
	issn = {0022-1767},
	year = {2013},
	eissn = {1550-6606},
	pages = {2036-2048},
	orcid-numbers = {Takeda, Akira/0000-0003-4748-4543; Suematsu, Makoto/0000-0002-7165-6336}
}

@article{MTMT:26413675,
	title = {Lysophosphatidic Acid Enhances Stromal Cell-Directed Angiogenesis},
	url = {https://m2.mtmt.hu/api/publication/26413675},
	author = {Binder, Bernard Y K and Sondergaard, Claus S and Nolta, Jan A and Leach, J Kent},
	doi = {10.1371/journal.pone.0082134},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {8},
	unique-id = {26413675},
	year = {2013},
	eissn = {1932-6203}
}

@article{MTMT:2756700,
	title = {Role of the autotaxin-lysophosphatidate axis in cancer resistance to chemotherapy and radiotherapy.},
	url = {https://m2.mtmt.hu/api/publication/2756700},
	author = {Brindley, DN and Lin, FT and Tigyi, Gabor},
	doi = {10.1016/j.bbalip.2012.08.015},
	journal-iso = {BBA-MOL CELL BIOL L},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS},
	volume = {1831},
	unique-id = {2756700},
	issn = {1388-1981},
	abstract = {High expression of autotaxin in cancers is often associated with increased tumor progression, angiogenesis and metastasis. This is explained mainly since autotaxin produces the lipid growth factor, lysophosphatidate (LPA), which stimulates cell division, survival and migration. It has recently become evident that these signaling effects of LPA also produce resistance to chemotherapy and radiation-induced cell death. This results especially from the stimulation of LPA(2) receptors, which depletes the cell of Siva-1, a pro-apoptotic signaling protein and stimulates prosurvival kinase pathways through a mechanism mediated via TRIP-6. LPA signaling also increases the formation of sphingosine 1-phosphate, a pro-survival lipid. At the same time, LPA decreases the accumulation of ceramides, which are used in radiation therapy and by many chemotherapeutic agents to stimulate apoptosis. The signaling actions of extracellular LPA are terminated by its dephosphorylation by a family of lipid phosphate phosphatases (LPP) that act as ecto-enzymes. In addition, lipid phosphate phoshatase-1 attenuates signaling downstream of the activation of both LPA receptors and receptor tyrosine kinases. This makes many cancer cells hypersensitive to the action of various growth factors since they often express low LPP1/3 activity. Increasing our understanding of the complicated signaling pathways that are used by LPA to stimulate cell survival should identify new therapeutic targets that can be exploited to increase the efficacy of chemo- and radio-therapy. This article is part of a Special Issue entitled Advances in Lysophospholipid Research.},
	keywords = {Animals; Humans; signal transduction; *Drug Resistance, Neoplasm; Phosphoric Diester Hydrolases/*metabolism; *Radiation Tolerance; Receptors, Lysophosphatidic Acid/metabolism; Neoplasms/*drug therapy/metabolism/*radiotherapy; Lysophospholipids/*metabolism},
	year = {2013},
	eissn = {1879-2618},
	pages = {74-85},
	orcid-numbers = {Tigyi, Gabor/0000-0001-5371-171X}
}

@article{MTMT:26417212,
	title = {Development of lysophosphatidic acid pathway modulators as therapies for fibrosis},
	url = {https://m2.mtmt.hu/api/publication/26417212},
	author = {Budd, David C and Qian, Yimin},
	doi = {10.4155/FMC.13.154},
	journal-iso = {FUTURE MED CHEM},
	journal = {FUTURE MEDICINAL CHEMISTRY},
	volume = {5},
	unique-id = {26417212},
	issn = {1756-8919},
	year = {2013},
	eissn = {1756-8927},
	pages = {1935-1952}
}