@{MTMT:32020552,
	title = {Helyi hormonok (autakoidok): hisztamin, antihisztaminok, szerotoninreceptor-agonisták és -antagonisták, prosztaglandinok},
	url = {https://m2.mtmt.hu/api/publication/32020552},
	author = {Pethő, Gábor and Szolcsányi, János},
	booktitle = {Farmakológia és klinikai farmakológia},
	unique-id = {32020552},
	year = {2020},
	pages = {644-664}
}

@{MTMT:31684068,
	title = {Resolvin D1 and D2 inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel activation on sensory neurons via lipid raft modification},
	url = {https://m2.mtmt.hu/api/publication/31684068},
	author = {Payrits, Maja and Ádám, Horváth and Biró-Sütő, Tünde and János, Erostyák and Géza, Makkai and Sághy, Éva and Pohóczky, Krisztina and Kecskés, Angéla and Kecskés, Miklós and Szolcsányi, János and Helyes, Zsuzsanna and Szőke, Éva},
	booktitle = {Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project},
	unique-id = {31684068},
	year = {2020},
	pages = {59-59},
	orcid-numbers = {Sághy, Éva/0000-0002-4031-3461; Pohóczky, Krisztina/0000-0003-0385-5162}
}

@article{MTMT:31625361,
	title = {In vitro and in vivo evidence for the role of lipid rafts in Ca2+-gating of the Transient Receptor Potential channels in sensory neurons},
	url = {https://m2.mtmt.hu/api/publication/31625361},
	author = {Szőke, Éva and Horvath, Adam and Biró-Sütő, Tünde and Sághy, Éva and Payrits, Maja and Erostyák, János and Makkai, Géza and Szolcsányi, János and Helyes, Zsuzsanna},
	doi = {10.1096/fasebj.2020.34.s1.05167},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {34},
	unique-id = {31625361},
	issn = {0892-6638},
	keywords = {Biology; Biochemistry & Molecular Biology},
	year = {2020},
	eissn = {1530-6860},
	orcid-numbers = {Sághy, Éva/0000-0002-4031-3461}
}

@article{MTMT:31396188,
	title = {Small molecule somatostatin receptor subtype 4 (sst4) agonists are novel anti-inflammatory and analgesic drug candidates},
	url = {https://m2.mtmt.hu/api/publication/31396188},
	author = {Szőke, Éva and Bálint, Mónika Enikő and Hetényi, Csaba and Markovics, Adrienn and Elekes, Krisztián and Pozsgai, Gábor and Szűts, Tamás and Kéri, György and Őrfi, László and Sándor, Zoltán and Szolcsányi, János and Pintér, Erika and Helyes, Zsuzsanna},
	doi = {10.1016/j.neuropharm.2020.108198},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {178},
	unique-id = {31396188},
	issn = {0028-3908},
	abstract = {We provided strong proof of concept evidence that somatostatin mediates potent analgesic and anti-inflammatory actions via its receptor subtype 4 (sst4) located both at the periphery and the central nervous system. Therefore, sst4 agonists are promising novel drug candidates for neuropathic pain and neurogenic inflammation, but rational drug design was not possible due to the lack of knowledge about its 3-dimensional structure. We modeled the sst4 receptor structure, described its agonist binding properties, and characterized the binding of our novel small molecule sst4 agonists (4-phenetylamino-7H-pyrrolo[2,3-d]pyrimidine derivatives) using an in silico platform. In addition to the in silico binding data, somatostatin displacement by Compound 1 was demonstrated in the competitive binding assay on sst4-expressing cells. In vivo effects were investigated in rat models of neurogenic inflammation and chronic traumatic neuropathic pain. We defined high- and low-affinity binding pockets of sst4 for our ligands, binding of the highest affinity compounds were similar to that of the reference ligand J-2156. We showed potent G-protein activation with the highest potency of 10 nM EC50 value and highest efficacy of 342%. Oral administration of 100 μg/kg of 5 compounds significantly inhibited acute neurogenic plasma protein extravasation in the paw skin by 40-60%, one candidate abolished and 3 others diminished sciatic nerve-ligation induced neuropathic hyperalgesia by 28-62%. The in silico predictions on sst4-ligands were tested in biological systems. Low oral dose of our novel agonists inhibit neurogenic inflammation and neuropathic pain, which opens promising drug developmental perspectives for these unmet medical need conditions.},
	keywords = {Inflammation; SOMATOSTATIN; Neuropathic pain; somatostatin receptor subtype 4; Analgesic drug; Anti-inflammatory drug},
	year = {2020},
	eissn = {1873-7064},
	orcid-numbers = {Őrfi, László/0000-0001-6149-2385; Pintér, Erika/0000-0001-9898-632X}
}

@article{MTMT:31387590,
	title = {Resolvin D1 and D2 inhibit transient receptor potential vanilloid 1 and ankyrin 1 ion channel activation on sensory neurons via lipid raft modification},
	url = {https://m2.mtmt.hu/api/publication/31387590},
	author = {Payrits, Maja and Horváth, Ádám and Biró-Sütő, Tünde and Erostyák, János and Makkai, Géza and Sághy, Éva and Pohóczky, Krisztina and Kecskés, Angéla and Kecskés, Miklós and Szolcsányi, János and Helyes, Zsuzsanna and Szőke, Éva},
	doi = {10.3390/ijms21145019},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31387590},
	issn = {1661-6596},
	abstract = {Transient Receptor Potential Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons and regulate nociceptor and inflammatory functions. Resolvins are endogenous lipid mediators. Resolvin D1 (RvD1) is described as a selective inhibitor of TRPA1-related postoperative and inflammatory pain in mice acting on the G protein-coupled receptor DRV1/GPR32. Resolvin D2 (RvD2) is a very potent TRPV1 and TRPA1 inhibitor in DRG neurons, and decreases inflammatory pain in mice acting on the GPR18 receptor, via TRPV1/TRPA1-independent mechanisms. We provided evidence that resolvins inhibited neuropeptide release from the stimulated sensory nerve terminals by TRPV1 and TRPA1 activators capsaicin (CAPS) and allyl-isothiocyanate (AITC), respectively. We showed that RvD1 and RvD2 in nanomolar concentrations significantly decreased TRPV1 and TRPA1 activation on sensory neurons by fluorescent calcium imaging and inhibited the CAPS-and AITC-evoked45Ca-uptake on TRPV1-and TRPA1-expressing CHO cells. Since CHO cells are unlikely to express resolvin receptors, resolvins are suggested to inhibit channel opening through surrounding lipid raft disruption. Here, we proved the ability of resolvins to alter the membrane polarity related to cholesterol composition by fluorescence spectroscopy. It is concluded that targeting lipid raft integrity can open novel peripheral analgesic opportunities by decreasing the activation of nociceptors. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {LIPID RAFTS; transient receptor potential channel; sensory neuron; resolvin D1; nerve terminal; Resolvin D2},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Sághy, Éva/0000-0002-4031-3461; Pohóczky, Krisztina/0000-0003-0385-5162}
}

@article{MTMT:30306941,
	title = {Complex Role of Capsaicin-Sensitive Afferents in the Collagen Antibody-Induced Autoimmune Arthritis of the Mouse},
	url = {https://m2.mtmt.hu/api/publication/30306941},
	author = {Borbély, Éva and Kiss, Tamás and Szabadfi, Krisztina and Pintér, Erika and Szolcsányi, János and Helyes, Zsuzsanna and Botz, Bálint},
	doi = {10.1038/s41598-018-34005-6},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {8},
	unique-id = {30306941},
	issn = {2045-2322},
	abstract = {Capsaicin-sensitive afferents have complex regulatory functions in the joints orchestrated via neuropeptides. This study aimed to determine their role in the collagen-antibody induced rheumatoid arthritis model. Capsaicin-sensitive nerves were defunctionalized by the capsaicin receptor agonist resiniferatoxin in C57Bl/6 mice. Arthritis was induced by the ArithroMab antibody cocktail and adjuvant. Arthritis was monitored by measuring body weight, joint edema by plethysmometry, arthritis severity by clinical scoring, mechanonociceptive threshold by plantar esthesiometry, thermonociceptive threshold by hot plate, cold tolerance by paw withdrawal latency from 0 °C water. Grasping ability was determined by the wire-grid grip test. Bone structure was evaluated by in vivo micro-CT and histology. Arthritic animals developed a modest joint edema, mechanical and cold hyperalgesia, weight loss, and a diminished grasping function, while thermal hyperalgesia is absent in the model. Desensitised mice displayed reduced arthritis severity, edema, and mechanical hyperalgesia, however, cold hyperalgesia was significantly greater in this group. Arthritic controls displayed a transient decrease of bone volume and an increased porosity, while bone density and trabecularity increased in desensitised mice. The activation of capsaicin-sensitive afferents increases joint inflammation and mechanical hyperalgesia, but decreases cold allodynia. It also affects inflammatory bone structural changes by promoting bone resorption.},
	keywords = {SERUM; RESINIFERATOXIN; SUBSTANCE-P; PAIN; RHEUMATOID-ARTHRITIS; ANIMAL-MODELS; INDUCED INFLAMMATION; KNEE-JOINT; rat},
	year = {2018},
	eissn = {2045-2322},
	orcid-numbers = {Borbély, Éva/0000-0002-1234-4391; Pintér, Erika/0000-0001-9898-632X}
}

@article{MTMT:3402940,
	title = {Carboxamido steroids inhibit the opening properties of Transient Receptor Potential ion channels by lipid raft modulation.},
	url = {https://m2.mtmt.hu/api/publication/3402940},
	author = {Sághy, Éva and Payrits, Maja and Biro-Suto, T and Skodáné Földes, Rita and Szánti-Pintér, Eszter and Erostyák, János and Makkai, Géza and Sétáló, György (ifj.) and Kollár, László and Kőszegi, Tamás and Jakabfi-Csepregi, Rita and Szolcsányi, János and Helyes, Zsuzsanna and Szőke, Éva},
	doi = {10.1194/jlr.M084723},
	journal-iso = {J LIPID RES},
	journal = {JOURNAL OF LIPID RESEARCH},
	volume = {59},
	unique-id = {3402940},
	issn = {0022-2275},
	abstract = {Transient Receptor Potential (TRP) cation channels, like the TRP Vanilloid 1 and TRP Ankyrin 1 (TRPV1 and TRPA1) are expressed on primary sensory neurons. These thermosensor channels play role in pain processing. We provided evidence that lipid raft disruption influenced the TRP channel activation and a carboxamido-steroid compound (C1) inhibited TRPV1 activation. Therefore, our aim was to investigate whether this compound exerts its effect through lipid raft disruption and the steroid backbone (C3) or altered position of the carboxamido group (C2) influence the inhibitory action by measuring Ca2+-transients on isolated neurons and calcium-uptake on receptor-expressing CHO cells. Membrane cholesterol content was measured by filipin staining and membrane polarisation by fluorescence spectroscopy. Both the percentage of responsive cells and the magnitude of the intracellular Ca2+-enhancement evoked by the TRPV1 agonist capsaicin were significantly inhibited after C1 and C2 incubation, but not after C3 administration. C1 was able to reduce other TRP channel activation as well. The compounds induced cholesterol depletion in CHO cells, but only C1 induced changes in membrane polarisation. The inhibitory action of the compounds on TRP channel activation develops by lipid raft disruption, and the presence and the position of the carboxamido group is essential.},
	keywords = {CELL-LINE; ACTIVATION; NICOTINIC ACETYLCHOLINE-RECEPTOR; ROOT GANGLION NEURONS; LIPID RAFTS; steroid; transient receptor potential channel; TRPV1 receptor; sensory neuron; Cation channels; nerve terminal; TRIGEMINAL SENSORY NEURONS; ALPHA-SPINASTEROL; SCREEN REVEALS},
	year = {2018},
	eissn = {1539-7262},
	pages = {1851-1863},
	orcid-numbers = {Sághy, Éva/0000-0002-4031-3461; Skodáné Földes, Rita/0000-0002-9810-1509; Szánti-Pintér, Eszter/0000-0001-8263-9884}
}

@article{MTMT:3339990,
	title = {Upregulation of extraneuronal TRPV1 expression in chronic rhinosinusitis with nasal polyps},
	url = {https://m2.mtmt.hu/api/publication/3339990},
	author = {Tóth, Eszter and Tornóczky, Tamás and Kneif, Józsefné and Perkecz, A and Katona, Krisztián and Piski, Zalán and Kemény, Ágnes and Gerlinger, Imre and Szolcsányi, János and Kun, József and Pintér, Erika},
	doi = {10.4193/Rhin17.108},
	journal-iso = {RHINOLOGY},
	journal = {RHINOLOGY},
	volume = {56},
	unique-id = {3339990},
	issn = {0300-0729},
	abstract = {BACKGROUND: Chronic rhinosinusitis (CRS) is a multifactorial upper airway disease with unclear etiology. Neuronal Transient Receptor Potential Vanilloid 1 (TRPV1) and Ankyrin 1 (TRPA1) channels have been implicated in the pathogenesis of CRS. We aimed to detect the expression of extraneuronal TRPV1 and TRPA1 receptors in nasal polyp (NP) tissue samples. METHODOLOGY: Samples were obtained from fourty-two CRS pateints with nasal polyp and sixteen healthy controls to measure receptor gene expression by quantitative PCR, protein localization by immunohistochemistry and cytokine profile by multiplex bead immunoassay. RESULTS: Non-neuronal TRPV1, TRPA1 receptors were expressed in biopsy samples of NP. A population of mast cells and macrophages were immunopositive for TRPV1 and TRPA1. A fraction of plasma cells expressed TRPV1 but not TRPA1 and neither receptor was present on eosinophils. The local gene expression of extraneuronal TRPV1, TRPA1 receptors was also proven. TRPV1 mRNA levels were significantly increased in CRSwNP patients with asthma and allergic rhinitis compared to their NP counterparts. CONCLUSIONS: Elevated TRPV1 levels in comorbid asthma and allergy may have a function in CRSwNP. Subpopulation-specific TRPV1 presence on plasma and mast cells can indicate delicate roles in regulating activation and release of inflammatory mediators.},
	year = {2018},
	eissn = {0300-0729},
	pages = {245-254},
	orcid-numbers = {Piski, Zalán/0000-0003-2592-9652; Kemény, Ágnes/0000-0002-4523-3938; Pintér, Erika/0000-0001-9898-632X}
}

@article{MTMT:3297015,
	title = {Nils Alwall a művese egyik alaptípusának feltalálója és magyar kapcsolata},
	url = {https://m2.mtmt.hu/api/publication/3297015},
	author = {Karátson, András and Szolcsányi, János},
	journal-iso = {HYPERTONIA NEPHROLOGIA},
	journal = {HYPERTONIA ÉS NEPHROLOGIA},
	volume = {21},
	unique-id = {3297015},
	issn = {1418-477X},
	year = {2017},
	eissn = {2498-6259},
	pages = {44-48}
}

@article{MTMT:3248672,
	title = {Estradiol sensitizes the Transient Receptor Potential Vanilloid 1 receptor in pain responses},
	url = {https://m2.mtmt.hu/api/publication/3248672},
	author = {Payrits, Maja and Sághy, Éva and Csekő, Kata and Pohóczky, Krisztina and Bölcskei, Kata and Ernszt, Dávid and Barabás, Klaudia and Szolcsányi, János and Ábrahám, István and Helyes, Zsuzsanna and Szőke, Éva},
	doi = {10.1210/en.2017-00101},
	journal-iso = {ENDOCRINOLOGY},
	journal = {ENDOCRINOLOGY},
	volume = {158},
	unique-id = {3248672},
	issn = {0013-7227},
	year = {2017},
	eissn = {1945-7170},
	pages = {3249-3258},
	orcid-numbers = {Sághy, Éva/0000-0002-4031-3461; Pohóczky, Krisztina/0000-0003-0385-5162}
}