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10.1093/hmg/ddw341 http://scihub22266oqcxt.onion/10.1093/hmg/ddw341 C5886043!5886043!27742777     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hum+Mol+Genet 2016 ; 25 (23): 5212-22 Nephropedia Template TP {{tp|p=27742777|t=2016. PNPLA3 overexpression results in reduction of proteins predisposing to fibrosis |pdf=|usr=}}{{27742777}} gab.com Text PNPLA3 overexpression results in reduction of proteins predisposing to fibrosis JO: Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=27742777 #FOAvip Liver fibrosis is a pathological scarring response to chronic hepatocellular injury and hepatic stellate cells (HSCs) are key players in this process. PNPLA3 I148M is a common variant robustly associated with liver fibrosis but the mechanisms underlying this association are unknown. We aimed to examine a) the effect of fibrogenic and proliferative stimuli on PNPLA3 levels in HSCs and b) the role of wild type and mutant PNPLA3 overexpression on markers of HSC activation and fibrosis.Here, we show that PNPLA3 is upregulated by the fibrogenic cytokine transforming growth factor-beta (TGF-?), but not by platelet-derived growth factor (PDGF), and is involved in the TGF-?-induced reduction in lipid droplets in primary human HSCs. Furthermore, we show that retinol release from human HSCs ex vivo is lower in cells with the loss-of-function PNPLA3 148M compared with 148I wild type protein. Stable overexpression of PNPLA3 148I wild type, but not 148M mutant, in human HSCs (LX-2 cells) induces a reduction in the secretion of matrix metallopeptidase 2 (MMP2), tissue inhibitor of metalloproteinase 1 and 2 (TIMP1 and TIMP2), which is mediated by retinoid metabolism. In conclusion, we show a role for PNPLA3 in HSC activation in response to fibrogenic stimuli. Moreover, we provide evidence to indicate that PNPLA3-mediated retinol release may protect against liver fibrosis by inducing a specific signature of proteins involved in extracellular matrix remodelling. Twit Text FOAVip PNPLA3 overexpression results in reduction of proteins predisposing to fibrosis ????Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=27742777 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27742777 #FOAvip English Wikipedia <ref>{{Cite pmid|27742777}}</ref> PNPLA3 overexpression results in reduction of proteins predisposing to fibrosis #MMPMID27742777 Pingitore P; Dongiovanni P; Motta BM; Meroni M; Lepore SM; Mancina RM; Pelusi S; Russo C; Caddeo A; Rossi G; Montalcini T; Pujia A; Wiklund O; Valenti L; Romeo S Hum Mol Genet 2016[Dec]; 25 (23): 5212-22 PMID27742777show ga Liver fibrosis is a pathological scarring response to chronic hepatocellular injury and hepatic stellate cells (HSCs) are key players in this process. PNPLA3 I148M is a common variant robustly associated with liver fibrosis but the mechanisms underlying this association are unknown. We aimed to examine a) the effect of fibrogenic and proliferative stimuli on PNPLA3 levels in HSCs and b) the role of wild type and mutant PNPLA3 overexpression on markers of HSC activation and fibrosis.Here, we show that PNPLA3 is upregulated by the fibrogenic cytokine transforming growth factor-beta (TGF-?), but not by platelet-derived growth factor (PDGF), and is involved in the TGF-?-induced reduction in lipid droplets in primary human HSCs. Furthermore, we show that retinol release from human HSCs ex vivo is lower in cells with the loss-of-function PNPLA3 148M compared with 148I wild type protein. Stable overexpression of PNPLA3 148I wild type, but not 148M mutant, in human HSCs (LX-2 cells) induces a reduction in the secretion of matrix metallopeptidase 2 (MMP2), tissue inhibitor of metalloproteinase 1 and 2 (TIMP1 and TIMP2), which is mediated by retinoid metabolism. In conclusion, we show a role for PNPLA3 in HSC activation in response to fibrogenic stimuli. Moreover, we provide evidence to indicate that PNPLA3-mediated retinol release may protect against liver fibrosis by inducing a specific signature of proteins involved in extracellular matrix remodelling. äPNPLA3 overexpression results in reduction of proteins predisposing to(epmc).pdf DeepDyve Pubget Overpricing