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10.1016/j.yjmcc.2015.01.006 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2015.01.006 C4346432!4346432!25633835     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 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       J+Mol+Cell+Cardiol 2015 ; 80 (ä): 175-85 Nephropedia Template TP {{tp|p=25633835|t=2015. Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation |pdf=|usr=}}{{25633835}} gab.com Text Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=25633835 #FOAvip Thickening of mitral leaflets, endothelial-to-mesenchymal transition (EndMT), and activated myofibroblast-like interstitial cells have been observed in ischemic mitral valve regurgitation. We set out to determine if interactions between mitral valve endothelial cells (VEC) and interstitial cells (VIC) might affect these alterations. We used in vitro co-culture in Transwell? inserts to test the hypothesis that VIC secrete factors that inhibit EndMT and conversely, that VEC secrete factors that mitigate the activation of VIC to a myofibroblast-like, activated phenotype. Primary cultures and clonal populations of ovine mitral VIC and VEC were used. Western blot, quantitative reverse transcriptase PCR (qPCR) and functional assays were used to assess changes in cell phenotype and behavior. VIC or conditioned media from VIC inhibited transforming growth factor? (TGF?)-induced EndMT in VEC, as indicated by reduced expression of EndMT markers ?-smooth muscle actin (?-SMA), Slug, Snai1 and MMP-2 and maintained ability of VEC to mediate leukocyte adhesion, an important endothelial function. VEC or conditioned media from VEC reversed the spontaneous cell culture-induced change in VIC to an activated phenotype, as indicated by reduced expression of ?-SMA and type I collagen, increased expression chondromodulin-1 (Chm1), and reduced contractile activity. These results demonstrate that mitral VEC and VIC secrete soluble factors that can reduce VIC activation and inhibit TGF?-driven EndMT, respectively. These findings suggest that the endothelium of the mitral valve is critical for the maintenance of a quiescent VIC phenotype and that, in turn, VIC prevent EndMT. We speculate that disturbance of the ongoing reciprocal interactions between VEC and VICs in vivo may contribute to the thickened and fibrotic leaflets observed in ischemic mitral regurgitation, and in other types of valve disease. Twit Text FOAVip Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=25633835 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25633835 #FOAvip English Wikipedia <ref>{{Cite pmid|25633835}}</ref> Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation #MMPMID25633835 Shapero K; Wylie-Sears J; Levine RA; Mayer JE; Bischoff J J Mol Cell Cardiol 2015[Mar]; 80 (ä): 175-85 PMID25633835show ga Thickening of mitral leaflets, endothelial-to-mesenchymal transition (EndMT), and activated myofibroblast-like interstitial cells have been observed in ischemic mitral valve regurgitation. We set out to determine if interactions between mitral valve endothelial cells (VEC) and interstitial cells (VIC) might affect these alterations. We used in vitro co-culture in Transwell? inserts to test the hypothesis that VIC secrete factors that inhibit EndMT and conversely, that VEC secrete factors that mitigate the activation of VIC to a myofibroblast-like, activated phenotype. Primary cultures and clonal populations of ovine mitral VIC and VEC were used. Western blot, quantitative reverse transcriptase PCR (qPCR) and functional assays were used to assess changes in cell phenotype and behavior. VIC or conditioned media from VIC inhibited transforming growth factor? (TGF?)-induced EndMT in VEC, as indicated by reduced expression of EndMT markers ?-smooth muscle actin (?-SMA), Slug, Snai1 and MMP-2 and maintained ability of VEC to mediate leukocyte adhesion, an important endothelial function. VEC or conditioned media from VEC reversed the spontaneous cell culture-induced change in VIC to an activated phenotype, as indicated by reduced expression of ?-SMA and type I collagen, increased expression chondromodulin-1 (Chm1), and reduced contractile activity. These results demonstrate that mitral VEC and VIC secrete soluble factors that can reduce VIC activation and inhibit TGF?-driven EndMT, respectively. These findings suggest that the endothelium of the mitral valve is critical for the maintenance of a quiescent VIC phenotype and that, in turn, VIC prevent EndMT. We speculate that disturbance of the ongoing reciprocal interactions between VEC and VICs in vivo may contribute to the thickened and fibrotic leaflets observed in ischemic mitral regurgitation, and in other types of valve disease. äReciprocal interactions between mitral valve endothelial and interstit(epmc).pdf DeepDyve Pubget Overpricing