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http://scihub22266oqcxt.onion/ C5482276!5482276!28649665     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       New+Front+Ophthalmol 2017 ; 3 (1): ä Nephropedia Template TP {{tp|p=28649665|t=2017. TGF-?-target genes are differentially regulated in corneal epithelial cells and fibroblasts |pdf=|usr=}}{{28649665}} gab.com Text TGF- -target genes are differentially regulated in corneal epithelial cells and fibroblasts JO: New Front Ophthalmol http://www.kidney.de/pget.php?&tw=1&pmid=28649665 #FOAvip Purpose: Transforming growth factor-beta (TGF-?) activates the canonical Smad pathway, which includes the Smad family of proteins and SARA (Smad Anchor for Receptor Activation) and other less understood pathways, including one involving p38MAPK. The goal of the current research was to determine if corneal epithelial cells and fibroblasts used the classical or alternative TGF-?-signaling pathways. To examine this question, we made use of Trx-SARA, which inhibits native SARA, thus blocking the Smad pathway. Methods: A human corneal epithelial cell line (HCE-TJ), and stromal fibroblasts (HCF) were infected with retroviruses (RTV) containing either Trx-SARA or Trx-GA (a control plasmid). The effect of Trx-SARA on thrombospondin-1 (TSP-1) expression in both cell types, p15ink4b expression in HCE-TJ, and cellular fibronectin (cFN) expression in HCF was determined. In addition, the effect of p38MAPK inhibitor on TSP-1 and p15ink4b were examined. Results: In HCE-TJ with TGF-?1, TSP-1-protein levels increased and peaked at 24 hours. Trx-SARA reduced TSP-1 expression in HCE-TJ, but had no effect on p15ink4b. With HCF, Trx-SARA failed to reduce TSP-1 expression; however, cFN expression decreased and proliferation was inhibited. By blocking the p38MAPK pathway, TSP-1 expression was reduced in HCF and p15ink4b expression was decreased in HCE-TJ. Conclusions: Surprisingly, TSP-1 was regulated through the Smad pathway in HCE-TJ and the p38MAPK pathway in HCF. The p38MAPK pathway also induced p15ink4b in HCE-TJ. Our results indicate that not all TGF-?-target proteins require the Smad pathway, and it may be possible to block certain TGF-?-target proteins without blocking the expression of all the TGF-?-target proteins. Twit Text FOAVip TGF- -target genes are differentially regulated in corneal epithelial cells and fibroblasts ????New Front Ophthalmol http://www.kidney.de/pget.php?&tw=1&pmid=28649665 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28649665 #FOAvip English Wikipedia <ref>{{Cite pmid|28649665}}</ref> TGF-?-target genes are differentially regulated in corneal epithelial cells and fibroblasts #MMPMID28649665 Guo X; Hutcheon AEK; Tran JA; Zieske JD New Front Ophthalmol 2017[]; 3 (1): ä PMID28649665show ga Purpose: Transforming growth factor-beta (TGF-?) activates the canonical Smad pathway, which includes the Smad family of proteins and SARA (Smad Anchor for Receptor Activation) and other less understood pathways, including one involving p38MAPK. The goal of the current research was to determine if corneal epithelial cells and fibroblasts used the classical or alternative TGF-?-signaling pathways. To examine this question, we made use of Trx-SARA, which inhibits native SARA, thus blocking the Smad pathway. Methods: A human corneal epithelial cell line (HCE-TJ), and stromal fibroblasts (HCF) were infected with retroviruses (RTV) containing either Trx-SARA or Trx-GA (a control plasmid). The effect of Trx-SARA on thrombospondin-1 (TSP-1) expression in both cell types, p15ink4b expression in HCE-TJ, and cellular fibronectin (cFN) expression in HCF was determined. In addition, the effect of p38MAPK inhibitor on TSP-1 and p15ink4b were examined. Results: In HCE-TJ with TGF-?1, TSP-1-protein levels increased and peaked at 24 hours. Trx-SARA reduced TSP-1 expression in HCE-TJ, but had no effect on p15ink4b. With HCF, Trx-SARA failed to reduce TSP-1 expression; however, cFN expression decreased and proliferation was inhibited. By blocking the p38MAPK pathway, TSP-1 expression was reduced in HCF and p15ink4b expression was decreased in HCE-TJ. Conclusions: Surprisingly, TSP-1 was regulated through the Smad pathway in HCE-TJ and the p38MAPK pathway in HCF. The p38MAPK pathway also induced p15ink4b in HCE-TJ. Our results indicate that not all TGF-?-target proteins require the Smad pathway, and it may be possible to block certain TGF-?-target proteins without blocking the expression of all the TGF-?-target proteins. äTGF-?-target genes are differentially regulated in corneal epithelial (epmc).pdf DeepDyve Pubget Overpricing