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10.1038/srep15857 http://scihub22266oqcxt.onion/10.1038/srep15857 C4629142!4629142!26522369     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26522369&cmd=llinks): Failed to open stream: HTTP request failed! 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Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload |pdf=|usr=}}{{26522369}} gab.com Text Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26522369 #FOAvip Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD+) biosynthesis, and thereby regulates the deacetylase activity of sirtuins. Here we show accommodative regulation of myocardial NAD+ by monocyte-derived extracellular Nampt (eNampt), which is essential for hemodynamic compensation to pressure overload. Although intracellular Nampt (iNampt) expression was decreased in pressure-overloaded hearts, myocardial NAD+ concentration and Sirt1 activity were preserved. In contrast, iNampt was up-regulated in spleen and monocytes, and circulating eNampt protein and nicotinamide mononucleotide (NMN), a key precursor of NAD+, were significantly increased. Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD+ levels and NAD+-dependent Sirt1 activity, leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice. These biochemical and hemodynamic defects were prevented by systemic administration of NMN. Our studies uncover a crucial role of monocyte-derived eNampt in myocardial adaptation to pressure overload, and highlight a potential intervention controlling myocardial NAD+ against heart failure. Twit Text FOAVip Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26522369 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26522369 #FOAvip English Wikipedia <ref>{{Cite pmid|26522369}}</ref> Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ protects the heart against pressure overload #MMPMID26522369 Yano M; Akazawa H; Oka T; Yabumoto C; Kudo-Sakamoto Y; Kamo T; Shimizu Y; Yagi H; Naito AT; Lee JK; Suzuki Ji; Sakata Y; Komuro I Sci Rep 2015[]; 5 (ä): ä PMID26522369show ga Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD+) biosynthesis, and thereby regulates the deacetylase activity of sirtuins. Here we show accommodative regulation of myocardial NAD+ by monocyte-derived extracellular Nampt (eNampt), which is essential for hemodynamic compensation to pressure overload. Although intracellular Nampt (iNampt) expression was decreased in pressure-overloaded hearts, myocardial NAD+ concentration and Sirt1 activity were preserved. In contrast, iNampt was up-regulated in spleen and monocytes, and circulating eNampt protein and nicotinamide mononucleotide (NMN), a key precursor of NAD+, were significantly increased. Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD+ levels and NAD+-dependent Sirt1 activity, leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice. These biochemical and hemodynamic defects were prevented by systemic administration of NMN. Our studies uncover a crucial role of monocyte-derived eNampt in myocardial adaptation to pressure overload, and highlight a potential intervention controlling myocardial NAD+ against heart failure. äMonocyte-derived extracellular Nampt-dependent biosynthesis of NAD+ pr(epmc).pdf DeepDyve Pubget Overpricing