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10.1016/j.bbrc.2014.03.014 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2014.03.014 C4007266!4007266!24632204     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 282.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 282.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 282.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochem+Biophys+Res+Commun 2014 ; 446 (4): 870-5 Nephropedia Template TP {{tp|p=24632204|t=2014. Losartan Inhibits Endothelial-to-Mesenchymal Transformation in Mitral Valve Endothelial Cells by Blocking Transforming Growth Factor-?-induced Phosphorylation of ERK |pdf=|usr=}}{{24632204}} gab.com Text Losartan Inhibits Endothelial-to-Mesenchymal Transformation in Mitral Valve Endothelial Cells by Blocking Transforming Growth Factor- -induced Phosphorylation of ERK JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=24632204 #FOAvip Adult cardiac valve endothelial cells (VEC) undergo endothelial to mesenchymal transformation (EndMT) in response to transforming growth factor-? (TGF?). EndMT has been proposed as a mechanism to replenish interstitial cells that reside within the leaflets and further, as an adaptive response that increases the size of mitral valve leaflets after myocardial infarction. To better understand valvular EndMT, we investigated TGF?-induced signaling in mitral VEC, and carotid artery endothelial cells (CAEC) as a control. Expression of EndMT target genes ?-smooth muscle actin (?-SMA), Snai1, Slug, and MMP-2 were used to monitor EndMT. We show that TGF?-induced EndMT increases phosphorylation of ERK (p-ERK), and this is blocked by Losartan, an FDA-approved antagonist of the angiotensin II type 1 receptor (AT1), that is known to indirectly inhibit phosphorylation of ERK (p-ERK). Blocking TGF-?-induced p-ERK directly with the MEK1/2 inhibitor RDEA119 was sufficient to prevent EndMT. In mitral VECs, TGF? had only modest effects on phosphorylation of the canonical TGF-? signaling mediator mothers against decapentaplegic homolog 3 (SMAD3). These results indicate a predominance of the non-canonical p-ERK pathway in TGF?-mediated EndMT in mitral VECs. AT1 and angiotensin II type 2 (AT2) were detected in mitral VEC, and high concentrations of angiotensin II (AngII) stimulated EndMT, which was blocked by Losartan. The ability of Losartan or MEK1/2 inhibitors to block EndMT suggests these drugs may be useful in manipulating EndMT to prevent excessive growth and fibrosis that occurs in the leaflets after myocardial infarction. Twit Text FOAVip Losartan Inhibits Endothelial-to-Mesenchymal Transformation in Mitral Valve Endothelial Cells by Blocking Transforming Growth Factor- -induced Phosphorylation of ERK ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=24632204 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24632204 #FOAvip English Wikipedia <ref>{{Cite pmid|24632204}}</ref> Losartan Inhibits Endothelial-to-Mesenchymal Transformation in Mitral Valve Endothelial Cells by Blocking Transforming Growth Factor-?-induced Phosphorylation of ERK #MMPMID24632204 Wylie-Sears J; Levine R; Bischoff J Biochem Biophys Res Commun 2014[Apr]; 446 (4): 870-5 PMID24632204show ga Adult cardiac valve endothelial cells (VEC) undergo endothelial to mesenchymal transformation (EndMT) in response to transforming growth factor-? (TGF?). EndMT has been proposed as a mechanism to replenish interstitial cells that reside within the leaflets and further, as an adaptive response that increases the size of mitral valve leaflets after myocardial infarction. To better understand valvular EndMT, we investigated TGF?-induced signaling in mitral VEC, and carotid artery endothelial cells (CAEC) as a control. Expression of EndMT target genes ?-smooth muscle actin (?-SMA), Snai1, Slug, and MMP-2 were used to monitor EndMT. We show that TGF?-induced EndMT increases phosphorylation of ERK (p-ERK), and this is blocked by Losartan, an FDA-approved antagonist of the angiotensin II type 1 receptor (AT1), that is known to indirectly inhibit phosphorylation of ERK (p-ERK). Blocking TGF-?-induced p-ERK directly with the MEK1/2 inhibitor RDEA119 was sufficient to prevent EndMT. In mitral VECs, TGF? had only modest effects on phosphorylation of the canonical TGF-? signaling mediator mothers against decapentaplegic homolog 3 (SMAD3). These results indicate a predominance of the non-canonical p-ERK pathway in TGF?-mediated EndMT in mitral VECs. AT1 and angiotensin II type 2 (AT2) were detected in mitral VEC, and high concentrations of angiotensin II (AngII) stimulated EndMT, which was blocked by Losartan. The ability of Losartan or MEK1/2 inhibitors to block EndMT suggests these drugs may be useful in manipulating EndMT to prevent excessive growth and fibrosis that occurs in the leaflets after myocardial infarction. äLosartan Inhibits Endothelial-to-Mesenchymal Transformation in Mitral (epmc).pdf DeepDyve Pubget Overpricing