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10.3892/mmr.2017.7356 http://scihub22266oqcxt.onion/10.3892/mmr.2017.7356 C5865756!5865756!28849131     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 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Med+Rep 2017 ; 16 (5): 5752-8 Nephropedia Template TP {{tp|p=28849131|t=2017. Periostin cross-reacts with the renin-angiotensin system during liver fibrosis development |pdf=|usr=}}{{28849131}} gab.com Text Periostin cross-reacts with the renin-angiotensin system during liver fibrosis development JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28849131 #FOAvip Periostin is a 90-kDa extracellular matrix protein, which is secreted primarily from fibroblasts and is expressed in the lungs, kidneys and heart valves. Angiotensin II (AT-II) serves pivotal roles in the pathogenesis of several diseases with accompanying fibrosis, including chronic liver diseases. AT-II induces periostin expression by regulating transforming growth factor-?1 (TGF-?1)/Smad signaling during cardiac fibrosis. The aim of the present study was to investigate the interaction between AT-II and periostin during liver fibrosis development. Fischer 344 rats were fed a choline-deficient L-amino-acid (CDAA)-defined diet for 12 weeks to simulate the development of steatohepatitis with liver fibrosis. Losartan, an AT-II type I receptor blocker, was administered to inhibit the effect of AT-II. The therapeutic effect of losartan on hepatic fibrosis development and on periostin expression was then evaluated. Several in vitro experiments were performed to examine the mechanisms underlying the interaction between AT-II and periostin in activated hepatic stellate cells (Ac-HSCs). Treatment with losartan suppressed the development of liver fibrosis induced by the CDAA diet, and reduced hepatic periostin expression. In addition, losartan treatment suppressed hepatic Ac-HSC expansion and hepatic TGF-?1 expression. In vitro analysis using LX2 HSC cells indicated that AT-II can augment TGF-?1 and collagen type I ?1 mRNA expression via periostin expression, suggesting that the interaction between AT-II and periostin may serve a role in liver fibrosis development. In conclusion, blockade of AT-II-induced periostin may suppress the progression of liver fibrosis development. Twit Text FOAVip Periostin cross-reacts with the renin-angiotensin system during liver fibrosis development ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28849131 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28849131 #FOAvip English Wikipedia <ref>{{Cite pmid|28849131}}</ref> Periostin cross-reacts with the renin-angiotensin system during liver fibrosis development #MMPMID28849131 Takeda K; Noguchi R; Kitade M; Namisaki T; Moriya K; Kawaratani H; Okura Y; Kaji K; Aihara Y; Douhara A; Nishimura N; Sawada Y; Seki K; Yoshiji H Mol Med Rep 2017[Nov]; 16 (5): 5752-8 PMID28849131show ga Periostin is a 90-kDa extracellular matrix protein, which is secreted primarily from fibroblasts and is expressed in the lungs, kidneys and heart valves. Angiotensin II (AT-II) serves pivotal roles in the pathogenesis of several diseases with accompanying fibrosis, including chronic liver diseases. AT-II induces periostin expression by regulating transforming growth factor-?1 (TGF-?1)/Smad signaling during cardiac fibrosis. The aim of the present study was to investigate the interaction between AT-II and periostin during liver fibrosis development. Fischer 344 rats were fed a choline-deficient L-amino-acid (CDAA)-defined diet for 12 weeks to simulate the development of steatohepatitis with liver fibrosis. Losartan, an AT-II type I receptor blocker, was administered to inhibit the effect of AT-II. The therapeutic effect of losartan on hepatic fibrosis development and on periostin expression was then evaluated. Several in vitro experiments were performed to examine the mechanisms underlying the interaction between AT-II and periostin in activated hepatic stellate cells (Ac-HSCs). Treatment with losartan suppressed the development of liver fibrosis induced by the CDAA diet, and reduced hepatic periostin expression. In addition, losartan treatment suppressed hepatic Ac-HSC expansion and hepatic TGF-?1 expression. In vitro analysis using LX2 HSC cells indicated that AT-II can augment TGF-?1 and collagen type I ?1 mRNA expression via periostin expression, suggesting that the interaction between AT-II and periostin may serve a role in liver fibrosis development. In conclusion, blockade of AT-II-induced periostin may suppress the progression of liver fibrosis development. äPeriostin cross-reacts with the renin-angiotensin system during liver (epmc).pdf DeepDyve Pubget Overpricing