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10.1002/2211-5463.12202 http://scihub22266oqcxt.onion/10.1002/2211-5463.12202 C5377407!5377407!28396839     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       FEBS+Open+Bio 2017 ; 7 (4): 550-61 Nephropedia Template TP {{tp|p=28396839|t=2017. Inhibition of the TGF? signalling pathway by cGMP and cGMP?dependent kinase I in renal fibrosis |pdf=|usr=}}{{28396839}} gab.com Text Inhibition of the TGF signalling pathway by cGMP and cGMP dependent kinase I in renal fibrosis JO: FEBS Open Bio http://www.kidney.de/pget.php?&tw=1&pmid=28396839 #FOAvip Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic effects of cGMP and cGMP?dependent kinase I (cGKI) are mediated via regulation of the TGF? signalling pathway, both via ERK and the Smad?dependent route. Kidney fibrosis was induced by unilateral ureter obstruction (UUO) in wild?type and cGKI?deficient (cGKI?KO) mice. The cGMP/cGKI signalling pathway was activated by application of the soluble guanylate cyclase (sGC) stimulator BAY 41?8543 (BAY), beginning 1 day after UUO. After 7 days, the antifibrotic effects of BAY were analysed by measuring mRNA and protein expression of characteristic fibrotic biomarkers. The effects of cGMP/TGF? on cultured fibroblasts were also analysed in vitro. BAY application influenced the activity of the extracellular matrix (ECM)?degrading matrix metalloproteases (MMP2 and MMP9) and their inhibitor tissue inhibitors of metalloproteinase?1, the secretion of cytokines (e.g. IL?6) and the expression pattern of ECM proteins (e.g. collagen, fibronectin) and profibrotic mediators (e.g. connective tissue growth factors and plasminogen?activator inhibitor?1). Activation of the cGMP/cGKI signalling pathway showed protective effects against fibrosis which were mediated by inhibition of P?Erk1/2 and translocation of P?smad3. The elucidation of these signalling mechanisms might support the development of new therapeutic options regarding cGMP/cGKI?mediated antifibrotic actions. Twit Text FOAVip Inhibition of the TGF signalling pathway by cGMP and cGMP dependent kinase I in renal fibrosis ????FEBS Open Bio http://www.kidney.de/pget.php?&tw=1&pmid=28396839 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28396839 #FOAvip English Wikipedia <ref>{{Cite pmid|28396839}}</ref> Inhibition of the TGF? signalling pathway by cGMP and cGMP?dependent kinase I in renal fibrosis #MMPMID28396839 Schinner E; Wetzl V; Schramm A; Kees F; Sandner P; Stasch J; Hofmann F; Schlossmann J FEBS Open Bio 2017[Apr]; 7 (4): 550-61 PMID28396839show ga Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic effects of cGMP and cGMP?dependent kinase I (cGKI) are mediated via regulation of the TGF? signalling pathway, both via ERK and the Smad?dependent route. Kidney fibrosis was induced by unilateral ureter obstruction (UUO) in wild?type and cGKI?deficient (cGKI?KO) mice. The cGMP/cGKI signalling pathway was activated by application of the soluble guanylate cyclase (sGC) stimulator BAY 41?8543 (BAY), beginning 1 day after UUO. After 7 days, the antifibrotic effects of BAY were analysed by measuring mRNA and protein expression of characteristic fibrotic biomarkers. The effects of cGMP/TGF? on cultured fibroblasts were also analysed in vitro. BAY application influenced the activity of the extracellular matrix (ECM)?degrading matrix metalloproteases (MMP2 and MMP9) and their inhibitor tissue inhibitors of metalloproteinase?1, the secretion of cytokines (e.g. IL?6) and the expression pattern of ECM proteins (e.g. collagen, fibronectin) and profibrotic mediators (e.g. connective tissue growth factors and plasminogen?activator inhibitor?1). Activation of the cGMP/cGKI signalling pathway showed protective effects against fibrosis which were mediated by inhibition of P?Erk1/2 and translocation of P?smad3. The elucidation of these signalling mechanisms might support the development of new therapeutic options regarding cGMP/cGKI?mediated antifibrotic actions. äInhibition of the TGF? signalling pathway by cGMP and cGMP?dependent k(epmc).pdf DeepDyve Pubget Overpricing