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10.1038/s41598-017-01936-5 http://scihub22266oqcxt.onion/10.1038/s41598-017-01936-5 C5432493!5432493!28507335     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28507335|t=2017. BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through Ca2+ i-TGF-?-Smad2/3 pathway |pdf=|usr=}}{{28507335}} gab.com Text BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through Ca2+ i-TGF- -Smad2/3 pathway JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28507335 #FOAvip Fibrosis is an important, structurally damaging event that occurs in pathological cardiac remodeling, leading to cardiac dysfunction. BNIP3L is up-regulated in pressure overload-induced heart failure and has been reported to play an important role in cardiomyocyte apoptosis; however, its involvement in cardiac fibroblasts (CFs) remains unknown. We prove for the first time that the expression of BNIP3L is significantly increased in the CFs of rats undergoing pressure overload-induced heart failure. Furthermore, this increased BNIP3L expression was confirmed in cultured neonatal rat CFs undergoing proliferation and extracellular matrix (ECM) protein over-expression that was induced by norepinephrine (NE). The overexpression or suppression of BNIP3L promoted or inhibited NE-induced proliferation and ECM expression in CFs, respectively. In addition, [Ca2+]i, transforming growth factor beta (TGF-?) and the nuclear accumulation of Smad2/3 were successively increased when BNIP3L was overexpressed and reduced when BNIP3L was inhibited. Furthermore, the down-regulation of TGF-? by TGF-?-siRNA attenuated the increase of BNIP3L-induced fibronectin expression. We also demonstrated that the increase of BNIP3L in CFs was regulated by NE-AR-PKC pathway in vitro and in vivo. These results reveal that BNIP3L is a novel mediator of pressure overload-induced cardiac fibrosis through the [Ca2+]i-TGF-?-Smad2/3 pathway in CFs. Twit Text FOAVip BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through Ca2+ i-TGF- -Smad2/3 pathway ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28507335 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28507335 #FOAvip English Wikipedia <ref>{{Cite pmid|28507335}}</ref> BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through Ca2+ i-TGF-?-Smad2/3 pathway #MMPMID28507335 Liu W; Wang X; Mei Z; Gong J; Huang l; Gao X; Zhao Y; Ma J; Qian L Sci Rep 2017[]; 7 (ä): ä PMID28507335show ga Fibrosis is an important, structurally damaging event that occurs in pathological cardiac remodeling, leading to cardiac dysfunction. BNIP3L is up-regulated in pressure overload-induced heart failure and has been reported to play an important role in cardiomyocyte apoptosis; however, its involvement in cardiac fibroblasts (CFs) remains unknown. We prove for the first time that the expression of BNIP3L is significantly increased in the CFs of rats undergoing pressure overload-induced heart failure. Furthermore, this increased BNIP3L expression was confirmed in cultured neonatal rat CFs undergoing proliferation and extracellular matrix (ECM) protein over-expression that was induced by norepinephrine (NE). The overexpression or suppression of BNIP3L promoted or inhibited NE-induced proliferation and ECM expression in CFs, respectively. In addition, [Ca2+]i, transforming growth factor beta (TGF-?) and the nuclear accumulation of Smad2/3 were successively increased when BNIP3L was overexpressed and reduced when BNIP3L was inhibited. Furthermore, the down-regulation of TGF-? by TGF-?-siRNA attenuated the increase of BNIP3L-induced fibronectin expression. We also demonstrated that the increase of BNIP3L in CFs was regulated by NE-AR-PKC pathway in vitro and in vivo. These results reveal that BNIP3L is a novel mediator of pressure overload-induced cardiac fibrosis through the [Ca2+]i-TGF-?-Smad2/3 pathway in CFs. äBNIP3L promotes cardiac fibrosis in cardiac fibroblasts through Ca2+ (epmc).pdf DeepDyve Pubget Overpricing