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10.1371/journal.pone.0171093 http://scihub22266oqcxt.onion/10.1371/journal.pone.0171093 C5313173!5313173!28207769     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2017 ; 12 (2): ä Nephropedia Template TP {{tp|p=28207769|t=2017. Role of glycogen synthase kinase-3? and PPAR-? on epithelial-to-mesenchymal transition in DSS-induced colorectal fibrosis |pdf=|usr=}}{{28207769}} gab.com Text Role of glycogen synthase kinase-3 and PPAR- on epithelial-to-mesenchymal transition in DSS-induced colorectal fibrosis JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28207769 #FOAvip Background: Intestinal fibrosis is characterized by abnormal production and deposition of extracellular matrix (ECM) proteins by activated myofibroblasts. The main progenitor cells of activated myofibroblasts are the fibroblasts and the epithelial cells, the latter through the epithelial-mesenchymal transition (EMT). Aim: To evaluate the action of the new PPAR-? modulator, GED-0507-34 Levo (GED) on the expression of EMT associated and regulatory proteins such as TGF-?, Smad3, E-cadherin, Snail, ZEB1, ?-catenin, and GSK-3?, in a mouse model of DSS-induced intestinal fibrosis. Methods: Chronic colitis and fibrosis were induced by oral administration of 2.5% DSS (w/v) for 6 weeks. GW9662 (GW), a selective PPAR-? inhibitor, was also administered by intraperitoneal injection at the dose of 1 mg/kg/day combined with GED treatment. All drugs were administered at the beginning of the second cycle of DSS (day 12). 65 mice were randomly divided into five groups (H2O as controls n = 10, H2O+GED n = 10, DSS n = 15, DSS+GED n = 15, DSS+GED+GW n = 15). The colon was excised for macroscopic examination and histological and morphometric analyses. The level of expression of molecules involved in EMT and fibrosis, like TGF-?, Smad3, E-cadherin, Snail, ZEB1, ?-catenin, GSK-3? and PPAR-?, was assessed by immunohistochemistry, immunofluorescence, western blot and Real Time PCR. Results: GED improved the DSS-induced chronic colitis and fibrosis. GED was able to reduce the expression of the main fibrosis markers (?-SMA, collagen I-III and fibronectin) as well as the pivotal pro-fibrotic molecules IL-13, TGF-? and Smad3, while it increased the anti-fibrotic PPAR-?. All these GED effects were nullified by co-administration of GW with GED. Furthermore, GED was able to normalize the expression levels of E-cadherin and ?-catenin and upregulated GSK-3?, that are all known to be involved both in EMT and fibrosis. Conclusions: The DSS-induced intestinal fibrosis was improved by the new PPAR-? modulator GED-0507-34 Levo through the modulation of EMT mediators and pro-fibrotic molecules and through GSK-3? induction. Twit Text FOAVip Role of glycogen synthase kinase-3 and PPAR- on epithelial-to-mesenchymal transition in DSS-induced colorectal fibrosis ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28207769 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28207769 #FOAvip English Wikipedia <ref>{{Cite pmid|28207769}}</ref> Role of glycogen synthase kinase-3? and PPAR-? on epithelial-to-mesenchymal transition in DSS-induced colorectal fibrosis #MMPMID28207769 Di Gregorio J; Sferra R; Speca S; Vetuschi A; Dubuquoy C; Desreumaux P; Pompili S; Cristiano L; Gaudio E; Flati V; Latella G PLoS One 2017[]; 12 (2): ä PMID28207769show ga Background: Intestinal fibrosis is characterized by abnormal production and deposition of extracellular matrix (ECM) proteins by activated myofibroblasts. The main progenitor cells of activated myofibroblasts are the fibroblasts and the epithelial cells, the latter through the epithelial-mesenchymal transition (EMT). Aim: To evaluate the action of the new PPAR-? modulator, GED-0507-34 Levo (GED) on the expression of EMT associated and regulatory proteins such as TGF-?, Smad3, E-cadherin, Snail, ZEB1, ?-catenin, and GSK-3?, in a mouse model of DSS-induced intestinal fibrosis. Methods: Chronic colitis and fibrosis were induced by oral administration of 2.5% DSS (w/v) for 6 weeks. GW9662 (GW), a selective PPAR-? inhibitor, was also administered by intraperitoneal injection at the dose of 1 mg/kg/day combined with GED treatment. All drugs were administered at the beginning of the second cycle of DSS (day 12). 65 mice were randomly divided into five groups (H2O as controls n = 10, H2O+GED n = 10, DSS n = 15, DSS+GED n = 15, DSS+GED+GW n = 15). The colon was excised for macroscopic examination and histological and morphometric analyses. The level of expression of molecules involved in EMT and fibrosis, like TGF-?, Smad3, E-cadherin, Snail, ZEB1, ?-catenin, GSK-3? and PPAR-?, was assessed by immunohistochemistry, immunofluorescence, western blot and Real Time PCR. Results: GED improved the DSS-induced chronic colitis and fibrosis. GED was able to reduce the expression of the main fibrosis markers (?-SMA, collagen I-III and fibronectin) as well as the pivotal pro-fibrotic molecules IL-13, TGF-? and Smad3, while it increased the anti-fibrotic PPAR-?. All these GED effects were nullified by co-administration of GW with GED. Furthermore, GED was able to normalize the expression levels of E-cadherin and ?-catenin and upregulated GSK-3?, that are all known to be involved both in EMT and fibrosis. Conclusions: The DSS-induced intestinal fibrosis was improved by the new PPAR-? modulator GED-0507-34 Levo through the modulation of EMT mediators and pro-fibrotic molecules and through GSK-3? induction. äRole of glycogen synthase kinase-3? and PPAR-? on epithelial-to-mesenc(epmc).pdf DeepDyve Pubget Overpricing