@CONFERENCE{MTMT:34657419,
	title = {Defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis by the impaired regulation of PMCA activity},
	url = {https://m2.mtmt.hu/api/publication/34657419},
	author = {Madácsy, Tamara and Varga, Árpád and Csákány-Papp, Noémi and Tél, Bálint and Pallagi, Petra and Szabó, Viktória and Kiss, Aletta Kata and Fanczal, Júlia and Rakonczay, Zoltán and Tiszlavicz, László and Rázga, Zsolt and Hohweiler, Meike and Kleger, Alexander and Gray, Mike and Hegyi, Péter and Maléth, József},
	booktitle = {European Cystic Fibrosis Society 17th ECFS Basic Science Conference},
	unique-id = {34657419},
	year = {2022},
	pages = {135},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Csákány-Papp, Noémi/0000-0002-3614-2698; Tél, Bálint/0000-0003-2066-6494; Pallagi, Petra/0000-0001-8906-0840; Szabó, Viktória/0000-0001-6547-9102; Kiss, Aletta Kata/0000-0001-6404-1555; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Tiszlavicz, László/0000-0003-1134-6587; Rázga, Zsolt/0000-0003-4717-8482; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:32800045,
	title = {Impaired regulation of PMCA activity by defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis.},
	url = {https://m2.mtmt.hu/api/publication/32800045},
	author = {Madácsy, Tamara and Varga, Árpád and Csákány-Papp, Noémi and Tél, Bálint and Pallagi, Petra and Szabó, Viktória and Kiss, Aletta Kata and Fanczal, Júlia and Rakonczay, Zoltán and Tiszlavicz, László and Rázga, Zsolt and Hohwieler, Meike and Kleger, Alexander and Gray, Mike and Hegyi, Péter and Maléth, József},
	doi = {10.1007/s00018-022-04287-1},
	journal-iso = {CELL MOL LIFE SCI},
	journal = {CELLULAR AND MOLECULAR LIFE SCIENCES},
	volume = {79},
	unique-id = {32800045},
	issn = {1420-682X},
	abstract = {Alcoholic pancreatitis and hepatitis are frequent, potentially lethal diseases with limited treatment options. Our previous study reported that the expression of CFTR Cl- channel is impaired by ethanol in pancreatic ductal cells leading to more severe alcohol-induced pancreatitis. In addition to determining epithelial ion secretion, CFTR has multiple interactions with other proteins, which may influence intracellular Ca2+ signaling. Thus, we aimed to investigate the impact of ethanol-mediated CFTR damage on intracellular Ca2+ homeostasis in pancreatic ductal epithelial cells and cholangiocytes. Human and mouse pancreas and liver samples and organoids were used to study ion secretion, intracellular signaling, protein expression and interaction. The effect of PMCA4 inhibition was analyzed in a mouse model of alcohol-induced pancreatitis. The decreased CFTR expression impaired PMCA function and resulted in sustained intracellular Ca2+ elevation in ethanol-treated and mouse and human pancreatic organoids. Liver samples derived from alcoholic hepatitis patients and ethanol-treated mouse liver organoids showed decreased CFTR expression and function, and impaired PMCA4 activity. PMCA4 co-localizes and physically interacts with CFTR on the apical membrane of polarized epithelial cells, where CFTR-dependent calmodulin recruitment determines PMCA4 activity. The sustained intracellular Ca2+ elevation in the absence of CFTR inhibited mitochondrial function and was accompanied with increased apoptosis in pancreatic epithelial cells and PMCA4 inhibition increased the severity of alcohol-induced AP in mice. Our results suggest that improving Ca2+ extrusion in epithelial cells may be a potential novel therapeutic approach to protect the exocrine pancreatic function in alcoholic pancreatitis and prevent the development of cholestasis in alcoholic hepatitis.},
	keywords = {CFTR; Ca2+ signaling; Alcoholic pancreatitis; Alcoholic Hepatitis; Epithelial ion secretion},
	year = {2022},
	eissn = {1420-9071},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Csákány-Papp, Noémi/0000-0002-3614-2698; Tél, Bálint/0000-0003-2066-6494; Pallagi, Petra/0000-0001-8906-0840; Szabó, Viktória/0000-0001-6547-9102; Kiss, Aletta Kata/0000-0001-6404-1555; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Tiszlavicz, László/0000-0003-1134-6587; Rázga, Zsolt/0000-0003-4717-8482; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@misc{MTMT:32096788,
	title = {Decreased calmodulin recruitment triggers PMCA4 dysfunction and pancreatic injury in cystic fibrosis},
	url = {https://m2.mtmt.hu/api/publication/32096788},
	author = {Madácsy, Tamara and Varga, Árpád and Csákány-Papp, Noémi and Deák, Barnabás and Tél, Bálint and Pallagi, Petra and Szabó, Viktória and Fanczal, Júlia and Rakonczay, Zoltán and Rázga, Zsolt and Hohwieler, Meike and Kleger, Alexander and Gray, Mike and Hegyi, Péter and Maléth, József},
	unique-id = {32096788},
	abstract = {Exocrine pancreatic damage is a common complication of cystic fibrosis (CF), which can significantly debilitate the quality of life and life expectancy of CF patients. The cystic fibrosis transmembrane conductance regulator (CFTR) has a major role in pancreatic ductal ion secretion, however, it presumably has an influence on intracellular signaling as well. Here we describe in multiple model systems, including iPSC-derived human pancreatic organoids from CF patients, that the activity of PMCA4 is impaired by the decreased expression of CFTR in ductal cells. The regulation of PMCA4, which colocalizes and physically interacts with CFTR on the apical membrane of the ductal cells, is dependent on the calmodulin binding ability of CFTR. Moreover, CFTR seems to be involved in the process of the apical recruitment of calmodulin, which enhances its role in calcium signaling and homeostasis. Sustained intracellular Ca2+ elevation in CFTR KO cells undermined the mitochondrial function and increased apoptosis. Based on these, the prevention of sustained intracellular Ca2+ overload may improve the exocrine pancreatic function and may have a potential therapeutic aspect in CF.},
	year = {2020},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Csákány-Papp, Noémi/0000-0002-3614-2698; Tél, Bálint/0000-0003-2066-6494; Pallagi, Petra/0000-0001-8906-0840; Szabó, Viktória/0000-0001-6547-9102; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Rázga, Zsolt/0000-0003-4717-8482; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@mastersthesis{MTMT:31933101,
	title = {The role of intracellular Ca 2+ signaling in the exocrine pancreatic damage during acute pancreatitis [Az intracelluláris Ca2+ szignalizáció szerepe az exokrin hasnyálmirigy sejtek károsodásának kialakulásában heveny hasnyálmirigy gyulladás során]},
	url = {https://m2.mtmt.hu/api/publication/31933101},
	author = {Fanczal, Júlia},
	doi = {10.14232/phd.10488},
	publisher = {SZTE},
	unique-id = {31933101},
	year = {2020},
	orcid-numbers = {Fanczal, Júlia/0000-0001-7356-3857}
}

@{MTMT:31683899,
	title = {Investigation of the pancreatic ductal ion secretion in pancreatic ductal organoid cultures},
	url = {https://m2.mtmt.hu/api/publication/31683899},
	author = {Molnár, Réka and Fanczal, Júlia and Madácsy, Tamara and Hegyi, Péter and Maléth, József},
	booktitle = {Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project},
	unique-id = {31683899},
	year = {2020},
	pages = {18-18},
	orcid-numbers = {Molnár, Réka/0000-0002-3128-825X; Fanczal, Júlia/0000-0001-7356-3857; Madácsy, Tamara/0000-0001-5598-9723; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:31097108,
	title = {TRPM2-mediated extracellular Ca2+ entry promotes acinar cell necrosis in biliary acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/31097108},
	author = {Fanczal, Júlia and Pallagi, Petra and Görög, Marietta and Diszházi, Gyula and Almássy, János and Madácsy, Tamara and Varga, Árpád and Csernay-Biró, Péter and Katona, Xénia and Tóth, Emese and Molnár, Réka and Rakonczay, Zoltán and Hegyi, Péter and Maléth, József},
	doi = {10.1113/JP279047},
	journal-iso = {J PHYSIOL-LONDON},
	journal = {JOURNAL OF PHYSIOLOGY-LONDON},
	volume = {598},
	unique-id = {31097108},
	issn = {0022-3751},
	abstract = {Acute biliary pancreatitis is a significant clinical challenge as currently no specific pharmaceutical treatment exists. Intracellular Ca2+ overload, increased reactive oxygen species (ROS) production, mitochondrial damage and intra-acinar digestive enzyme activation caused by bile acids are hallmarks of acute biliary pancreatitis. 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. We demonstrated 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 H2 O2 treatment and contributed to bile acid-induced extracellular Ca2+ influx in acinar cells, which promoted acinar cell necrosis in vitro and in vivo. These results suggest that the inhibition of TRPM2 may be a potential treatment option for biliary pancreatitis.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 H2 O2 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 vitro independently 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. This article is protected by copyright. All rights reserved.},
	keywords = {Acute pancreatitis; bile acid; Ca2+ signalling; TRPM2 channel; epithelial ion transport; acinar cell necrosis},
	year = {2020},
	eissn = {1469-7793},
	pages = {1253-1270},
	orcid-numbers = {Fanczal, Júlia/0000-0001-7356-3857; Pallagi, Petra/0000-0001-8906-0840; Görög, Marietta/0000-0003-3615-3140; Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Katona, Xénia/0000-0002-6053-9097; Molnár, Réka/0000-0002-3128-825X; Rakonczay, Zoltán/0000-0002-1499-3416; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:30766190,
	title = {Mouse pancreatic ductal organoid culture as a relevant model to study exocrine pancreatic ion secretion},
	url = {https://m2.mtmt.hu/api/publication/30766190},
	author = {Molnár, Réka and Madácsy, Tamara and Varga, Árpád and Németh, Margit and Katona, Xénia and Görög, Marietta and Molnár, Brigitta and Fanczal, Júlia and Rakonczay, Zoltán and Hegyi, Péter and Pallagi, Petra and Maléth, József},
	doi = {10.1038/s41374-019-0300-3},
	journal-iso = {LAB INVEST},
	journal = {LABORATORY INVESTIGATION},
	volume = {100},
	unique-id = {30766190},
	issn = {0023-6837},
	abstract = {Pancreatic exocrine secretory processes are challenging to investigate on primary epithelial cells. Pancreatic organoid cultures may help to overcome shortcomings of the current models, however the ion secretory processes in pancreatic organoids-and therefore their physiological relevance or their utility in disease modeling-are not known. To answer these questions, we provide side-by-side comparison of gene expression, morphology, and function of epithelial cells in primary isolated pancreatic ducts and organoids. We used mouse pancreatic ductal fragments for experiments or were grown in Matrigel to obtain organoid cultures. Using PCR analysis we showed that gene expression of ion channels and transporters remarkably overlap in primary ductal cells and organoids. Morphological analysis with scanning electron microscopy revealed that pancreatic organoids form polarized monolayers with brush border on the apical membrane. Whereas the expression and localization of key proteins involved in ductal secretion (cystic fibrosis transmembrane conductance regulator, Na+/H+ exchanger 1 and electrogenic Na+/HCO3- cotransporter 1) are equivalent to the primary ductal fragments. Measurements of intracellular pH and Cl- levels revealed no significant difference in the activities of the apical Cl-/HCO3- exchange, or in the basolateral Na+ dependent HCO3- uptake. In summary we found that ion transport activities in the mouse pancreatic organoids are remarkably similar to those observed in freshly isolated primary ductal fragments. These results suggest that organoids can be suitable and robust model to study pancreatic ductal epithelial ion transport in health and diseases and facilitate drug development for secretory pancreatic disorders like cystic fibrosis, or chronic pancreatitis.},
	year = {2020},
	eissn = {1530-0307},
	pages = {84-97},
	orcid-numbers = {Molnár, Réka/0000-0002-3128-825X; Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Katona, Xénia/0000-0002-6053-9097; Görög, Marietta/0000-0003-3615-3140; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Hegyi, Péter/0000-0003-0399-7259; Pallagi, Petra/0000-0001-8906-0840; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:31399002,
	title = {Characterization of the function of transient receptor potentialmelastatin 2 in mouse pancreas},
	url = {https://m2.mtmt.hu/api/publication/31399002},
	author = {Fanczal, Júlia and Pallagi, Petra and Görög, Marietta and Péter Bíró, Csaba and Madácsy, Tamara and Varga, Árpád and Rakonczay, Zoltán and Hegyi, Péter and Maléth, József},
	doi = {10.1016/j.pan.2019.05.249},
	journal-iso = {PANCREATOLOGY},
	journal = {PANCREATOLOGY},
	volume = {19},
	unique-id = {31399002},
	issn = {1424-3903},
	year = {2019},
	eissn = {1424-3911},
	pages = {S94-S94},
	orcid-numbers = {Fanczal, Júlia/0000-0001-7356-3857; Pallagi, Petra/0000-0001-8906-0840; Görög, Marietta/0000-0003-3615-3140; Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Rakonczay, Zoltán/0000-0002-1499-3416; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:31398797,
	title = {Pancreatic ductal organoid cultures are a suitable model to studypancreatic ductal ion secretion},
	url = {https://m2.mtmt.hu/api/publication/31398797},
	author = {Molnár, Réka and Görög, Marietta and Fanczal, Júlia and Madácsy, Tamara and Németh, Margit and Varga, Árpád and Katona, Xénia and Rakonczay, Zoltán and Hegyi, Péter and Pallagi, Petra and Maléth, József},
	doi = {10.1016/j.pan.2019.05.039},
	journal-iso = {PANCREATOLOGY},
	journal = {PANCREATOLOGY},
	volume = {19},
	unique-id = {31398797},
	issn = {1424-3903},
	year = {2019},
	eissn = {1424-3911},
	pages = {S18-S18},
	orcid-numbers = {Molnár, Réka/0000-0002-3128-825X; Görög, Marietta/0000-0003-3615-3140; Fanczal, Júlia/0000-0001-7356-3857; Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Katona, Xénia/0000-0002-6053-9097; Rakonczay, Zoltán/0000-0002-1499-3416; Hegyi, Péter/0000-0002-3128-825X; Pallagi, Petra/0000-0001-8906-0840; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:31398652,
	title = {PMCA pump dysfunction promotes Ca2+ overload and pancreaticductal epithelial cell damage in cysticfibrosis},
	url = {https://m2.mtmt.hu/api/publication/31398652},
	author = {Madácsy, Tamara and Varga, Árpád and Schmidt, Anna and Fanczal, Júlia and Pallagi, Petra and Rakonczay, Zoltán and Hegyi, Péter and Rázga, Zsolt and Kleger, Alexander and Gray, Mike and Németh, István and Maléth, József},
	doi = {10.1016/j.pan.2019.05.037},
	journal-iso = {PANCREATOLOGY},
	journal = {PANCREATOLOGY},
	volume = {19},
	unique-id = {31398652},
	issn = {1424-3903},
	year = {2019},
	eissn = {1424-3911},
	pages = {S17-S18},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Fanczal, Júlia/0000-0001-7356-3857; Pallagi, Petra/0000-0001-8906-0840; Rakonczay, Zoltán/0000-0002-1499-3416; Rázga, Zsolt/0000-0003-4717-8482; Maléth, József/0000-0001-5768-3090}
}