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10.1016/j.jacc.2016.01.030 http://scihub22266oqcxt.onion/10.1016/j.jacc.2016.01.030 C5887128!5887128!27150688     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       J+Am+Coll+Cardiol 2016 ; 67 (13): 1556-68 Nephropedia Template TP {{tp|p=27150688|t=2016. Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis |pdf=|usr=}}{{27150688}} gab.com Text Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis JO: J Am Coll Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=27150688 #FOAvip BACKGROUND: Cardiac fibrosis (CF) is associated with increased ventricular stiffness and diastolic dysfunction and is an independent predictor of long-term clinical outcomes of patients with heart failure (HF). We previously showed that the matricellular CCN5 protein is cardioprotective via its ability to inhibit CF and preserve cardiac contractility. OBJECTIVES: This study examined the role of CCN5 in human heart failure and tested whether CCN5 can reverse established CF in an experimental model of HF induced by pressure overload. METHODS: Human hearts were obtained from patients with end-stage heart failure. Extensive CF was induced by applying transverse aortic constriction for 8 weeks, which was followed by adeno-associated virus-mediated transfer of CCN5 to the heart. Eight weeks following gene transfer, cellular and molecular effects were examined. RESULTS: Expression of CCN5 was significantly decreased in failing hearts from patients with end-stage heart failure compared to nonfailing hearts. Trichrome staining and myofibroblast content measurements revealed that the established CF had been reversed by CCN5 gene transfer. Anti-CF effects of CCN5 were associated with inhibition of the transforming growth factor beta signaling pathway. CCN5 significantly inhibited endothelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation, which are 2 critical processes for CF progression, both in vivo and in vitro. In addition, CCN5 induced apoptosis in myofibroblasts, but not in cardiomyocytes or fibroblasts, both in vivo and in vitro. CCN5 provoked the intrinsic apoptotic pathway specifically in myofibroblasts, which may have been due the ability of CCN5 to inhibit the activity of NF?B, an antiapoptotic molecule. CONCLUSIONS: CCN5 can reverse established CF by inhibiting the generation of and enhancing apoptosis of myofibroblasts in the myocardium. CCN5 may provide a novel platform for the development of targeted anti-CF therapies. Twit Text FOAVip Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis ????J Am Coll Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=27150688 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27150688 #FOAvip English Wikipedia <ref>{{Cite pmid|27150688}}</ref> Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis #MMPMID27150688 Jeong D; Lee MA; Li Y; Yang DK; Kho C; Oh JG; Hong G; Lee A; Song MH; LaRocca TJ; Chen J; Liang L; Mitsuyama S; D?Escamard V; Kovacic JC; Kwak TH; Hajjar RJ; Park WJ J Am Coll Cardiol 2016[Apr]; 67 (13): 1556-68 PMID27150688show ga BACKGROUND: Cardiac fibrosis (CF) is associated with increased ventricular stiffness and diastolic dysfunction and is an independent predictor of long-term clinical outcomes of patients with heart failure (HF). We previously showed that the matricellular CCN5 protein is cardioprotective via its ability to inhibit CF and preserve cardiac contractility. OBJECTIVES: This study examined the role of CCN5 in human heart failure and tested whether CCN5 can reverse established CF in an experimental model of HF induced by pressure overload. METHODS: Human hearts were obtained from patients with end-stage heart failure. Extensive CF was induced by applying transverse aortic constriction for 8 weeks, which was followed by adeno-associated virus-mediated transfer of CCN5 to the heart. Eight weeks following gene transfer, cellular and molecular effects were examined. RESULTS: Expression of CCN5 was significantly decreased in failing hearts from patients with end-stage heart failure compared to nonfailing hearts. Trichrome staining and myofibroblast content measurements revealed that the established CF had been reversed by CCN5 gene transfer. Anti-CF effects of CCN5 were associated with inhibition of the transforming growth factor beta signaling pathway. CCN5 significantly inhibited endothelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation, which are 2 critical processes for CF progression, both in vivo and in vitro. In addition, CCN5 induced apoptosis in myofibroblasts, but not in cardiomyocytes or fibroblasts, both in vivo and in vitro. CCN5 provoked the intrinsic apoptotic pathway specifically in myofibroblasts, which may have been due the ability of CCN5 to inhibit the activity of NF?B, an antiapoptotic molecule. CONCLUSIONS: CCN5 can reverse established CF by inhibiting the generation of and enhancing apoptosis of myofibroblasts in the myocardium. CCN5 may provide a novel platform for the development of targeted anti-CF therapies. äMatricellular Protein CCN5 Reverses Established Cardiac Fibrosis (epmc).pdf DeepDyve Pubget Overpricing