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10.1038/s41598-017-05836-6 http://scihub22266oqcxt.onion/10.1038/s41598-017-05836-6 C5515908!5515908 !28720775     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28720775 &cmd=llinks): Failed to open stream: HTTP request failed! 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Metformin ameliorates the Phenotype Transition of Peritoneal Mesothelial Cells and Peritoneal Fibrosis via a modulation of Oxidative Stress |pdf=|usr=}}{{28720775 }} gab.com Text Metformin ameliorates the Phenotype Transition of Peritoneal Mesothelial Cells and Peritoneal Fibrosis via a modulation of Oxidative Stress JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28720775 #FOAvip Phenotype transition of peritoneum is an early mechanism of peritoneal fibrosis. Metformin, 5'-adenosine monophosphate-activated protein kinase (AMPK) activator, has recently received a new attention due to its preventive effect on organ fibrosis and cancer metastasis by inhibiting epithelial-to-mesenchymal transition (EMT). We investigated the effect of metformin on EMT of human peritoneal mesothelial cells (HPMC) and animal model of peritoneal dialysis (PD). TGF-?1-induced EMT in HPMC was ameliorated by metformin. Metformin alleviated NAPDH oxidase- and mitochondria-mediated ROS production with an increase in superoxide dismutase (SOD) activity and SOD2 expression. Metformin inhibited the activation of Smad2/3 and MAPK, GSK-3? phosphorylation, nuclear translocalization of ?-catenin and Snail in HPMCs. Effect of metformin on TGF-?1-induced EMT was ameliorated by either AMPK inhibitor or AMPK gene silencing. Another AMPK agonist, 5-amino-1-?-D-ribofuranosyl-imidazole-4-carboxamide partially blocked TGF-?1-induced EMT. In animal model of PD, intraperitoneal metformin decreased the peritoneal thickness and EMT with an increase in ratio of reduced to oxidized glutathione and the expression of SOD whereas it decreased the expression of nitrotyrosine and 8-hydroxy-2'-deoxyguanosine. Therefore, a modulation of AMPK in peritoneum can be a novel tool to prevent peritoneal fibrosis by providing a favorable oxidant/anti-oxidant milieu in peritoneal cavity and ameliorating phenotype transition of peritoneal mesothelial cells. Twit Text FOAVip Metformin ameliorates the Phenotype Transition of Peritoneal Mesothelial Cells and Peritoneal Fibrosis via a modulation of Oxidative Stress ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28720775 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28720775 #FOAvip English Wikipedia <ref>{{Cite pmid|28720775 }}</ref> Metformin ameliorates the Phenotype Transition of Peritoneal Mesothelial Cells and Peritoneal Fibrosis via a modulation of Oxidative Stress #MMPMID28720775 Shin HS ; Ko J ; Kim DA ; Ryu ES ; Ryu HM ; Park SH ; Kim YL ; Oh ES ; Kang DH Sci Rep 2017[Jul]; 7 (1 ): 5690 PMID28720775 show ga Phenotype transition of peritoneum is an early mechanism of peritoneal fibrosis. Metformin, 5'-adenosine monophosphate-activated protein kinase (AMPK) activator, has recently received a new attention due to its preventive effect on organ fibrosis and cancer metastasis by inhibiting epithelial-to-mesenchymal transition (EMT). We investigated the effect of metformin on EMT of human peritoneal mesothelial cells (HPMC) and animal model of peritoneal dialysis (PD). TGF-?1-induced EMT in HPMC was ameliorated by metformin. Metformin alleviated NAPDH oxidase- and mitochondria-mediated ROS production with an increase in superoxide dismutase (SOD) activity and SOD2 expression. Metformin inhibited the activation of Smad2/3 and MAPK, GSK-3? phosphorylation, nuclear translocalization of ?-catenin and Snail in HPMCs. Effect of metformin on TGF-?1-induced EMT was ameliorated by either AMPK inhibitor or AMPK gene silencing. Another AMPK agonist, 5-amino-1-?-D-ribofuranosyl-imidazole-4-carboxamide partially blocked TGF-?1-induced EMT. In animal model of PD, intraperitoneal metformin decreased the peritoneal thickness and EMT with an increase in ratio of reduced to oxidized glutathione and the expression of SOD whereas it decreased the expression of nitrotyrosine and 8-hydroxy-2'-deoxyguanosine. Therefore, a modulation of AMPK in peritoneum can be a novel tool to prevent peritoneal fibrosis by providing a favorable oxidant/anti-oxidant milieu in peritoneal cavity and ameliorating phenotype transition of peritoneal mesothelial cells. |AMP-Activated Protein Kinase Kinases [MESH] |Animals [MESH] |Cells, Cultured [MESH] |Disease Models, Animal [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Humans [MESH] |Metformin/*pharmacology [MESH] |Oxidative Stress/drug effects [MESH] |Peritoneal Dialysis/adverse effects [MESH] |Peritoneal Fibrosis/drug therapy [MESH] |Peritoneum/cytology/*drug effects [MESH] |Protein Kinases [MESH]Metformin ameliorates the Phenotype Transition of Peritoneal Mesotheli(epmc).pdf DeepDyve Pubget Overpricing