@mastersthesis{MTMT:33644854,
	title = {A glomeruloszklerózis korai és késői szakaszának vizsgálata rágcsálókban},
	url = {https://m2.mtmt.hu/api/publication/33644854},
	author = {Bukosza, Éva Nóra},
	doi = {10.14753/SE.2021.2448},
	unique-id = {33644854},
	year = {2021}
}

@article{MTMT:32708137,
	title = {Szemléletváltás küszöbén: új ismereteink a vesefibrosisról krónikus vesebetegségben},
	url = {https://m2.mtmt.hu/api/publication/32708137},
	author = {Bukosza, Éva Nóra},
	doi = {10.33668/HN.25.005},
	journal-iso = {HYPERTONIA NEPHROLOGIA},
	journal = {HYPERTONIA ÉS NEPHROLOGIA},
	volume = {25},
	unique-id = {32708137},
	issn = {1418-477X},
	abstract = {A krónikus vesebetegség a sokféle etiológia ellenére végső soron egységesen, a vese fibroticus átalakulási mechanizmusával vezet végstádiumú veseelégtelenséghez. Az elmúlt években született – elsősorban kísérletes – kutatási eredmények jelentősen megváltoztatták az elképzelést a vese ezen átalakulásával kapcsolatban: egyértelművé vált, hogy a vesefibrosis egy dinamikus, sok szereplő részvételével zajló aktív folyamat. Ezen folyamatokban részt vevő tényezők befolyásolása reményt jelenthet arra nézve, hogy képesek leszünk a krónikus vesebetegség végstádiumának megelőzésére. Ez az összefoglaló közlemény a vesefibrosis és a krónikus vesebetegség összefüggését, az elterjedt vizsgálómódszerekből származó eredményeket és a közelmúltban felismert paradigmaváltást hozó tényezőket mutatja be.},
	year = {2021},
	eissn = {2498-6259},
	pages = {53-60}
}

@article{MTMT:32122064,
	title = {Delayed Contralateral Nephrectomy Halted Post-Ischemic Renal Fibrosis Progression and Inhibited the Ischemia-Induced Fibromir Upregulation in Mice},
	url = {https://m2.mtmt.hu/api/publication/32122064},
	author = {Róka, Beáta and Tod, Pál and Kaucsár, Tamás and Bukosza, Éva Nóra and Vörös, Imre and Varga, Zoltán and Petrovich, Balázs and Ágg, Bence and Ferdinandy, Péter and Szénási, Gábor and Hamar, Péter},
	doi = {10.3390/biomedicines9070815},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {9},
	unique-id = {32122064},
	year = {2021},
	eissn = {2227-9059},
	orcid-numbers = {Róka, Beáta/0000-0002-1491-1644; Tod, Pál/0000-0001-9163-7071; Kaucsár, Tamás/0000-0003-4460-1265; Bukosza, Éva Nóra/0000-0001-7606-7824; Vörös, Imre/0000-0001-5922-6109; Varga, Zoltán/0000-0002-2758-0784; Petrovich, Balázs/0000-0002-9745-0416; Ágg, Bence/0000-0002-6492-0426; Ferdinandy, Péter/0000-0002-6424-6806; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:31332871,
	title = {Post-Ischemic Renal Fibrosis Progression Is Halted by Delayed Contralateral Nephrectomy : The Involvement of Macrophage Activation},
	url = {https://m2.mtmt.hu/api/publication/31332871},
	author = {Tod, Pál and Bukosza, Éva Nóra and Róka, Beáta and Kaucsár, Tamás and Fintha, Attila and Krenács, Tibor and Szénási, Gábor and Hamar, Péter},
	doi = {10.3390/ijms21113825},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31332871},
	issn = {1661-6596},
	abstract = {(1) Background: Successful treatment of acute kidney injury (AKI)-induced chronic kidney disease (CKD) is unresolved. We aimed to characterize the time-course of changes after contralateral nephrectomy (Nx) in a model of unilateral ischemic AKI-induced CKD with good translational utility. (2) Methods: Severe (30 min) left renal ischemia-reperfusion injury (IRI) or sham operation (S) was performed in male Naval Medical Research Institute (NMRI) mice followed by Nx or S one week later. Expression of proinflammatory, oxidative stress, injury and fibrotic markers was evaluated by RT-qPCR. (3) Results: Upon Nx, the injured kidney hardly functioned for three days, but it gradually regained function until day 14 to 21, as demonstrated by the plasma urea. Functional recovery led to a drastic reduction in inflammatory infiltration by macrophages and by decreases in macrophage chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) mRNA and most injury markers. However, without Nx, a marked upregulation of proinflammatory (TNF-α, IL-6, MCP-1 and complement-3 (C3)); oxidative stress (nuclear factor erythroid 2-related factor 2, NRF2) and fibrosis (collagen-1a1 (Col1a1) and fibronectin-1 (FN1)) genes perpetuated, and the injured kidney became completely fibrotic. Contralateral Nx delayed the development of renal failure up to 20 weeks. (4) Conclusion: Our results suggest that macrophage activation is involved in postischemic renal fibrosis, and it is drastically suppressed by contralateral nephrectomy ameliorating progression.},
	keywords = {Inflammation; MICE; chronic kidney disease; TNF-α; acute kidney injury; MCP-1},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Tod, Pál/0000-0001-9163-7071; Róka, Beáta/0000-0002-1491-1644; Kaucsár, Tamás/0000-0003-4460-1265; Fintha, Attila/0000-0002-0519-8170; Krenács, Tibor/0000-0001-9164-065X; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:31291830,
	title = {Podocyte RNA sequencing reveals Wnt- and ECM-associated genes as central in FSGS},
	url = {https://m2.mtmt.hu/api/publication/31291830},
	author = {Bukosza, Éva Nóra and Kratochwill, Klaus and Kornauth, Christoph and Schachner, Helga and Aufricht, Christoph and Gebeshuber, Christoph A.},
	doi = {10.1371/journal.pone.0231898},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {15},
	unique-id = {31291830},
	issn = {1932-6203},
	year = {2020},
	eissn = {1932-6203}
}

@article{MTMT:31257752,
	title = {ECM Characterization Reveals a Massive Activation of Acute Phase Response during FSGS.},
	url = {https://m2.mtmt.hu/api/publication/31257752},
	author = {Bukosza, Éva Nóra and Kornauth, Christoph and Hummel, Karin and Schachner, Helga and Huttary, Nicole and Krieger, Sigurd and Nöbauer, Katharina and Oszwald, André and Razzazi Fazeli, Ebrahim and Kratochwill, Klaus and Aufricht, Christoph and Szénási, Gábor and Hamar, Péter and Gebeshuber, Christoph A},
	doi = {10.3390/ijms21062095},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31257752},
	issn = {1661-6596},
	abstract = {The glomerular basement membrane (GBM) and extra-cellular matrix (ECM) are essential to maintain a functional interaction between the glomerular podocytes and the fenestrated endothelial cells in the formation of the slit diaphragm for the filtration of blood. Dysregulation of ECM homeostasis can cause Focal segmental glomerulosclerosis (FSGS). Despite this central role, alterations in ECM composition during FSGS have not been analyzed in detail yet. Here, we characterized the ECM proteome changes in miR-193a-overexpressing mice, which suffer from FSGS due to suppression of Wilms' tumor 1 (WT1). By mass spectrometry we identified a massive activation of the acute phase response, especially the complement and fibrinogen pathways. Several protease inhibitors (ITIH1, SERPINA1, SERPINA3) were also strongly increased. Complementary analysis of RNA expression data from both miR-193a mice and human FSGS patients identified additional candidate genes also mainly involved in the acute phase response. In total, we identified more than 60 dysregulated, ECM-associated genes with potential relevance for FSGS progression. Our comprehensive analysis of a murine FSGS model and translational comparison with human data offers novel targets for FSGS therapy.},
	keywords = {FIBRINOGEN; Complement system; SCLEROSIS; acute phase response; ECM; FSGS},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:31055164,
	title = {A systems pharmacology workflow with experimental validation to assess the potential of anakinra for treatment of focal and segmental glomerulosclerosis},
	url = {https://m2.mtmt.hu/api/publication/31055164},
	author = {Boehm, Michael and Bukosza, Éva Nóra and Huttary, Nicole and Herzog, Rebecca and Aufricht, Christoph and Kratochwill, Klaus and Gebeshuber, Christoph A.},
	doi = {10.1371/journal.pone.0214332},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {14},
	unique-id = {31055164},
	issn = {1932-6203},
	abstract = {Focal and Segmental Glomerulosclerosis (FSGS) is a severe glomerulopathy that frequently leads to end stage renal disease. Only a subset of patients responds to current therapies, making it important to identify alternative therapeutic options. The interleukin (IL)-1 receptor antagonist anakinra is beneficial in several diseases with renal involvement. Here, we evaluated the potential of anakinra for FSGS treatment. Molecular process models obtained from scientific literature data were used to build FSGS pathology and anakinra mechanism of action models by exploiting information on protein interactions. These molecular models were compared by statistical interference analysis and expert based molecular signature matching. Experimental validation was performed in Adriamycin- and lipopolysaccharide (LPS)-induced nephropathy mouse models. Interference analysis (containing 225 protein coding genes and 8 molecular process segments) of the FSGS molecular pathophysiology model with the drug mechanism of action of anakinra identified a statistically significant overlap with 43 shared molecular features that were enriched in pathways relevant in FSGS, such as plasminogen activating cascade, inflammation and apoptosis. Expert adjudication of molecular signature matching, focusing on molecular process segments did not suggest a high therapeutic potential of anakinra in FSGS. In line with this, experimental validation did not result in altered proteinuria or significant changes in expression of the FSGS-relevant genes COL1A1 and NPHS1. In summary, an integrated bioinformatic and experimental workflow showed that FSGS relevant molecular processes can be significantly affected by anakinra beyond the direct drug target IL-1 receptor type 1 (IL1R1) context but might not counteract central pathophysiology processes in FSGS. Anakinra is therefore not suggested for extended preclinical trials.},
	year = {2019},
	eissn = {1932-6203},
	orcid-numbers = {Herzog, Rebecca/0000-0003-1946-7770; Kratochwill, Klaus/0000-0003-0803-614X}
}

@article{MTMT:30789521,
	title = {Glomerular Collagen Deposition and Lipocalin-2 Expression Are Early Signs of Renal Injury in Prediabetic Obese Rats},
	url = {https://m2.mtmt.hu/api/publication/30789521},
	author = {Bukosza, Éva Nóra and Kaucsár, Tamás and Godó, Mária and Lajtár, Enikő and Tod, Pál and Koncsos, Gábor and Varga, Zoltán and Baranyai, Tamás and Nguyen, Minh Tu and Schachner, Helga and Sőti, Csaba and Ferdinandy, Péter and Giricz, Zoltán and Szénási, Gábor and Hamar, Péter},
	doi = {10.3390/ijms20174266},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {30789521},
	issn = {1661-6596},
	abstract = {Feeding rats with high-fat diet (HFD) with a single streptozotocin (STZ) injection induced obesity, slightly elevated fasting blood glucose and impaired glucose and insulin tolerance, and caused cardiac hypertrophy and mild diastolic dysfunction as published before by Koncsos et al. in 2016. Here we aimed to explore the renal consequences in the same groups of rats. Male Long-Evans rats were fed normal chow (CON; n = 9) or HFD containing 40% lard and were administered STZ at 20 mg/kg (i.p.) at week four (prediabetic rats, PRED, n = 9). At week 21 blood and urine samples were taken and kidney and liver samples were collected for histology, immunohistochemistry and for analysis of gene expression. HFD and STZ increased body weight and visceral adiposity and plasma leptin concentration. Despite hyperleptinemia, plasma C-reactive protein concentration decreased in PRED rats. Immunohistochemistry revealed elevated collagen IV protein expression in the glomeruli, and Lcn2 mRNA expression increased, while Il-1β mRNA expression decreased in both the renal cortex and medulla in PRED vs. CON rats. Kidney histology, urinary protein excretion, plasma creatinine, glomerular Feret diameter, desmin protein expression, and cortical and medullary mRNA expression of TGF-β1, Nrf2, and PPARγ were similar in CON and PRED rats. Reduced AMPKα phosphorylation of the autophagy regulator Akt was the first sign of liver damage, while plasma lipid and liver enzyme concentrations were similar. In conclusion, glomerular collagen deposition and increased lipocalin-2 expression were the early signs of kidney injury, while most biomarkers of inflammation, oxidative stress and fibrosis were negative in the kidneys of obese, prediabetic rats with mild heart and liver injury.},
	keywords = {Inflammation; OBESITY; Collagen Type IV; Lipocalin-2; Renal Injury},
	year = {2019},
	eissn = {1422-0067},
	orcid-numbers = {Kaucsár, Tamás/0000-0003-4460-1265; Tod, Pál/0000-0001-9163-7071; Koncsos, Gábor/0000-0001-5451-8719; Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Nguyen, Minh Tu/0000-0003-1653-8377; Sőti, Csaba/0000-0002-4057-7678; Ferdinandy, Péter/0000-0002-6424-6806; Giricz, Zoltán/0000-0003-2036-8665; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:30724853,
	title = {THE KIDNEY IS RELATIVELY RESISTANT TO OBESITY-RELATED COMORBIDITY IN PREDIABETIC LONG EVANS RATS FED A HIGH FAT DIET},
	url = {https://m2.mtmt.hu/api/publication/30724853},
	author = {Bukosza, Éva Nóra and Kaucsár, Tamás and Godó, Mária and Lajtár, Enikő and Tod, Pál and Koncsos, Gábor and Varga, Zoltán and Nguyen, Minhtu and Schachner, Helga and Sőti, Csaba and Giricz, Zoltán and Szénási, Gábor and Hamar, Péter},
	doi = {10.1093/ndt/gfz106.FP059},
	journal-iso = {NEPHROL DIAL TRANSPL},
	journal = {NEPHROLOGY DIALYSIS TRANSPLANTATION},
	volume = {34},
	unique-id = {30724853},
	issn = {0931-0509},
	abstract = {INTRODUCTION: We have shown previously that rats fed high fat diet with a single STZ injection developed obesity, prediabetes, cardiac hypertrophy, diastolic dysfunction and mild liver damage (Koncsos et al., 2016, Am J Physiol Heart Circ Physiol 311(4):H927-H943). The current study aimed to explore the renal consequences in the same groups of rats.METHODS: Male Long-Evans rats were fed normal chow (control; CON; n=9) or high-fat diet containing 40% lard and were administered streptozotocin (20 mg/kg, i.p.) at week four (prediabetic rats; PRED, n=9). At week 21 cardiac function was examined and blood and urine samples were collected for measuring urinary protein concentration, and serum urea, creatinine and leptin concentrations. Kidney samples were collected for histology, immunohistochemistry and mRNA expression.},
	year = {2019},
	eissn = {1460-2385},
	orcid-numbers = {Kaucsár, Tamás/0000-0003-4460-1265; Tod, Pál/0000-0001-9163-7071; Koncsos, Gábor/0000-0001-5451-8719; Varga, Zoltán/0000-0002-2758-0784; Sőti, Csaba/0000-0002-4057-7678; Giricz, Zoltán/0000-0003-2036-8665; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:27589080,
	title = {Lymphatic exosomes promote dendritic cell migration along guidance cues},
	url = {https://m2.mtmt.hu/api/publication/27589080},
	author = {Brown, Markus and Johnson, Louise A and Leone, Dario A and Majek, Peter and Vaahtomeri, Kari and Senfter, Daniel and Bukosza, Éva Nóra and Schachner, Helga and Asfour, Gabriele and Langer, Brigitte and Hauschild, Robert and Parapatics, Katja and Hong, Young-Kwon and Bennett, Keiryn L and Kain, Renate and Detmar, Michael and Sixt, Michael and Jackson, David G and Kerjaschki, Dontscho},
	doi = {10.1083/jcb.201612051},
	journal-iso = {J CELL BIOL},
	journal = {JOURNAL OF CELL BIOLOGY},
	volume = {217},
	unique-id = {27589080},
	issn = {0021-9525},
	abstract = {Lymphatic endothelial cells (LECs) release extracellular chemokines to guide the migration of dendritic cells. In this study, we report that LECs also release basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater numbers in the presence of inflammatory cytokines and accumulate in the perivascular stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic analyses of EEV fractions identified > 1,700 cargo proteins and revealed a dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion and enhanced the directional migratory response of human dendritic cells along guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory behavior and thus promote directional migration of CX3CR1-expressing cells in complex tissue environments. © 2018 Brown et al.},
	keywords = {ARTICLE; human; Cell Count; priority journal; controlled study; nonhuman; animal tissue; quantitative analysis; in vitro study; cellular distribution; Flow Cytometry; PROTEIN FUNCTION; Tumor Necrosis Factor; human tissue; cell migration; immunohistology; bioaccumulation; proteomics; ex vivo study; three dimensional imaging; Dendritic cell; cell function; exosome; CD63 antigen; cell labeling; immunoelectron microscopy; immunofluorescence microscopy; platelet endothelial cell adhesion molecule 1; fractalkine; CD9 antigen; lymph vessel endothelium},
	year = {2018},
	eissn = {1540-8140},
	pages = {2205-2221},
	orcid-numbers = {Vaahtomeri, Kari/0000-0001-7829-3518}
}