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001-es BibID:	BIBFORM082980
035-os BibID:	(WoS)000511350000001 (Scopus)85079060274 (PubMed)31917868
Első szerző:	Fanczal Júlia
Cím:	TRPM2-mediated extracellular Ca2+ entry promotes acinar cell necrosis in biliary acute pancreatitis / Júlia Fanczal, Petra Pallagi, Marietta Görög, Gyula Diszházi, János Almássy, Tamara Madácsy, Árpád Varga, Péter Csernay-Biró, Xénia Katona, Emese Tóth, Réka Molnár, Zoltán Rakonczay, Péter Hegyi, József Maléth
Dátum:	2020
ISSN:	0022-3751 1469-7793
Megjegyzések:	Acute biliary pancreatitis poses a significant clinical challenge as currently no specific pharmaceutical treatment exists. Disturbed intracellular Ca2+ signalling caused by bile acids is a hallmark of the disease, which induces increased reactive oxygen species (ROS) production, mitochondrial damage, intra-acinar digestive enzyme activation and cell death. Because of this mechanism of action, prevention of toxic cellular Ca2+ overload is a promising therapeutic target. Transient Receptor Potential Melastatin 2 (TRPM2) is a non-selective cation channel that has recently emerged as an important contributor to oxidative-stress-induced cellular Ca2+ overload across different diseases. However, the expression and possible functions of TRPM2 in the exocrine pancreas remain unknown. Here we found that TRPM2 is expressed in the plasma membrane of mouse pancreatic acinar and ductal cells, which can be activated by increased oxidative stress induced by H2O2 treatment. TRPM2 activity was found to contribute to bile acid-induced extracellular Ca2+ influx in acinar cells, but did not have the same effect in ductal cells. The generation of intracellular ROS in response to bile acids was remarkably higher in pancreatic acinar cells compared to isolated ducts, which can explain the difference between acinar and ductal cells. This activity promoted acinar cell necrosis in vitroindependently from mitochondrial damage or mitochondrial fragmentation. In addition, bile-acid-induced experimental pancreatitis was less severe in TRPM2 knockout mice, whereas the lack of TRPM2 had no protective effect in cerulein induced acute pancreatitis. Our results suggest that the inhibition of TRPM2 may be a potential treatment option for biliary pancreatitis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Ca2+ signalling TRPM2 channel acinar cell necrosis acute pancreatitis bile acid epithelial ion transport
Megjelenés:	Journal of Physiology. - 598 : 6 (2020), p. 1253-1270. -
További szerzők:	Pallagi Petra Görög Marietta Diszházi Gyula (1992-) (gyógyszerész) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Madácsy Tamara Varga Árpád Csernay-Biró Péter Katona Xénia Tóth Emese Molnár Réka Rakonczay Zoltán Hegyi Péter Jenő (belgyógyász) Maléth József
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001-es BibID:	BIBFORM049153
035-os BibID:	PMID:23907822
Első szerző:	Kemény Lajos V. (bőrgyógyász Szeged)
Cím:	Na+/Ca2+ exchangers regulate the migration and proliferation of human gastric myofibroblasts / Lajos V. Kemény, Andrea Schnúr, Mátyás Czepán, Zoltán Rakonczay, Jr., Eleonóra Gál, János Lonovics, György Lázár, Zsolt Simonka, Viktória Venglovecz, József Maléth, Linda Judák, István B. Németh, Kornélia Szabó, János Almássy, László Virág, Andrea Geisz, László Tiszlavicz, David I. Yule, Tibor Wittmann, Andrea Varró, Péter Hegyi
Dátum:	2013
Megjegyzések:	Gastrointestinal myofibroblasts are contractile, electrically nonexcitable, transitional cells that play a role in extracellular matrix production, in ulcer healing, and in pathophysiological conditions they contribute to chronic inflammation and tumor development. Na+/Ca2+ exchangers (NCX) are known to have a crucial role in Ca2+ homeostasis of contractile cells, however, no information is available concerning the role of NCX in the proliferation and migration of gastrointestinal myofibroblasts. In this study, our aim was to investigate the role of NCX in the Ca2+ homeostasis, migration, and proliferation of human gastrointestinal myofibroblasts, focusing on human gastric myofibroblasts (HGMs). We used microfluorometric measurements to investigate the intracellular Ca2+ and Na+ concentrations, PCR analysis and immunostaining to show the presence of the NCX, patch clamp for measuring NCX activity, and proliferation and migration assays to investigate the functional role of the exchanger. We showed that 53.0±8.1% of the HGMs present Ca2+ oscillations, which depend on extracellular Ca2+ and Na+, and can be inhibited by NCX inhibitors. NCX1, NCX2, and NCX3 were expressed at both mRNA and protein levels in HGMs, and they contribute to the intracellular Ca2+ and Na+ homeostasis as well, regardless of the oscillatory activity. NCX inhibitors significantly blocked the basal and insulin-like growth factor II-stimulated migration and proliferation rates of HGMs. In conclusion, we showed that NCX plays a pivotal role in regulating the Ca2+ homeostasis, migration, and proliferation of HGMs. The inhibition of NCX activity may be a potential therapeutic target in hyperproliferative gastric diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban calcium oscillation sodium-calcium exchanger human myofibroblast
Megjelenés:	American journal of physiology. Gastrointestinal and liver physiology. - 305 : 8 (2013), p. G552-G563. -
További szerzők:	Schnúr Andrea Czepán Mátyás Rakonczay Zoltán Jr. Gál Eleonóra Lonovics János (Szeged) Lázár György Simonka Zsolt Venglovecz Viktória Maléth József Judák Linda Németh István Balázs Szabó Kornélia Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Virág László (élettanász Szeged) Geisz Andrea Tiszlavicz László Yule, David I. Wittmann Tibor Varró Andrea Hegyi Péter Jenő (belgyógyász)
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