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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 J ; Sakata Y ; Komuro I Sci Rep 2015[Nov]; 5 (ä): 15857 PMID26522369 show 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. |Animals [MESH] |Cytokines/*metabolism [MESH] |Heart/*physiology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Monocytes/*metabolism [MESH] |Myocardium/metabolism [MESH] |NAD/*biosynthesis/*metabolism [MESH] |Nicotinamide Mononucleotide/metabolism [MESH] |Nicotinamide Phosphoribosyltransferase/*metabolism [MESH] |Protective Agents/*chemical synthesis/*metabolism [MESH] |Sirtuin 1/metabolism [MESH]Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD(+) (epmc).pdf DeepDyve Pubget Overpricing