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10.1371/journal.pone.0143802 http://scihub22266oqcxt.onion/10.1371/journal.pone.0143802 C4666639!4666639!26625141     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (12): ä Nephropedia Template TP {{tp|p=26625141|t=2015. Fn14, a Downstream Target of the TGF-? Signaling Pathway, Regulates Fibroblast Activation |pdf=|usr=}}{{26625141}} gab.com Text Fn14, a Downstream Target of the TGF- Signaling Pathway, Regulates Fibroblast Activation JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26625141 #FOAvip Fibrosis, the hallmark of human injuries and diseases such as serious burns, is characterized by excessive collagen synthesis and myofibroblast accumulation. Transforming growth factor-? (TGF-?), a potent inducer of collagen synthesis, has been implicated in fibrosis in animals. In addition to TGF-?, fibroblast growth factor-inducible molecule 14 (Fn14) has been reported to play an important role in fibrotic diseases, such as cardiac fibrosis. However, the function and detailed regulatory mechanism of Fn14 in fibrosis are unclear. Here, we investigated the effect of Fn14 on the activation of human dermal fibroblasts. In normal dermal fibroblasts, TGF-? signaling increased collagen production and Fn14 expression. Furthermore, Fn14 siRNA blocked extracellular matrix gene expression; even when TGF-? signaling was activated by TGF-?1, fibroblast activation remained blocked in the presence of Fn14 siRNA. Overexpressing Fn14 increased extracellular matrix gene expression. In determining the molecular regulatory mechanism, we discovered that SMAD4, an important TGF-? signaling co-mediator, bound to the Fn14 promoter and activated Fn14 transcription. Taken together, these results indicate that the TGF-? signaling pathway activates Fn14 expression through the transcription factor SMAD4 and that activated Fn14 expression increases extracellular matrix synthesis and fibroblast activation. Therefore, Fn14 may represent a promising approach to preventing the excessive accumulation of collagen or ECM in skin fibrosis. Twit Text FOAVip Fn14, a Downstream Target of the TGF- Signaling Pathway, Regulates Fibroblast Activation ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26625141 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26625141 #FOAvip English Wikipedia <ref>{{Cite pmid|26625141}}</ref> Fn14, a Downstream Target of the TGF-? Signaling Pathway, Regulates Fibroblast Activation #MMPMID26625141 Chen S; Liu J; Yang M; Lai W; Ye L; Chen J; Hou X; Ding H; Zhang W; Wu Y; Liu X; Huang S; Yu X; Xiao D PLoS One 2015[]; 10 (12): ä PMID26625141show ga Fibrosis, the hallmark of human injuries and diseases such as serious burns, is characterized by excessive collagen synthesis and myofibroblast accumulation. Transforming growth factor-? (TGF-?), a potent inducer of collagen synthesis, has been implicated in fibrosis in animals. In addition to TGF-?, fibroblast growth factor-inducible molecule 14 (Fn14) has been reported to play an important role in fibrotic diseases, such as cardiac fibrosis. However, the function and detailed regulatory mechanism of Fn14 in fibrosis are unclear. Here, we investigated the effect of Fn14 on the activation of human dermal fibroblasts. In normal dermal fibroblasts, TGF-? signaling increased collagen production and Fn14 expression. Furthermore, Fn14 siRNA blocked extracellular matrix gene expression; even when TGF-? signaling was activated by TGF-?1, fibroblast activation remained blocked in the presence of Fn14 siRNA. Overexpressing Fn14 increased extracellular matrix gene expression. In determining the molecular regulatory mechanism, we discovered that SMAD4, an important TGF-? signaling co-mediator, bound to the Fn14 promoter and activated Fn14 transcription. Taken together, these results indicate that the TGF-? signaling pathway activates Fn14 expression through the transcription factor SMAD4 and that activated Fn14 expression increases extracellular matrix synthesis and fibroblast activation. Therefore, Fn14 may represent a promising approach to preventing the excessive accumulation of collagen or ECM in skin fibrosis. äFn14, a Downstream Target of the TGF-? Signaling Pathway, Regulates Fi(epmc).pdf DeepDyve Pubget Overpricing