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10.1165/rcmb.2013-0187OC http://scihub22266oqcxt.onion/10.1165/rcmb.2013-0187OC C4068912!4068912 !24392990     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24392990 &cmd=llinks): Failed to open stream: HTTP request failed! 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Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase |pdf=|usr=}}{{24392990 }} gab.com Text Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=24392990 #FOAvip Recent studies have indicated that, during the development of pulmonary hypertension (PH), there is a switch from oxidative phosphorylation to glycolysis in the pulmonary endothelium. However, the mechanisms underlying this phenomenon have not been elucidated. Endothelin (ET)-1, an endothelial-derived vasoconstrictor peptide, is increased in PH, and has been shown to play an important role in the oxidative stress associated with PH. Thus, in this study, we investigated whether there was a potential link between increases in ET-1 and mitochondrial remodeling. Our data indicate that ET-1 induces the redistribution of endothelial nitric oxide synthase (eNOS) from the plasma membrane to the mitochondria in pulmonary arterial endothelial cells, and that this was dependent on eNOS uncoupling. We also found that ET-1 disturbed carnitine metabolism, resulting in the attenuation of mitochondrial bioenergetics. However, ATP levels were unchanged due to a compensatory increase in glycolysis. Further mechanistic investigations demonstrated that ET-1 mediated the redistribution of eNOS via the phosphorylation of eNOS at Thr495 by protein kinase C ?. In addition, the glycolytic switch appeared to be dependent on mitochondrial-derived reactive oxygen species that led to the activation of hypoxia-inducible factor signaling. Finally, the cell culture data were confirmed in vivo using the monocrotaline rat model of PH. Thus, we conclude that ET-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the redistribution of uncoupled eNOS to the mitochondria, and that preventing this event may be an approach for the treatment of PH. Twit Text FOAVip Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=24392990 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24392990 #FOAvip English Wikipedia <ref>{{Cite pmid|24392990 }}</ref> Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase #MMPMID24392990 Sun X ; Kumar S ; Sharma S ; Aggarwal S ; Lu Q ; Gross C ; Rafikova O ; Lee SG ; Dasarathy S ; Hou Y ; Meadows ML ; Han W ; Su Y ; Fineman JR ; Black SM Am J Respir Cell Mol Biol 2014[Jun]; 50 (6 ): 1084-95 PMID24392990 show ga Recent studies have indicated that, during the development of pulmonary hypertension (PH), there is a switch from oxidative phosphorylation to glycolysis in the pulmonary endothelium. However, the mechanisms underlying this phenomenon have not been elucidated. Endothelin (ET)-1, an endothelial-derived vasoconstrictor peptide, is increased in PH, and has been shown to play an important role in the oxidative stress associated with PH. Thus, in this study, we investigated whether there was a potential link between increases in ET-1 and mitochondrial remodeling. Our data indicate that ET-1 induces the redistribution of endothelial nitric oxide synthase (eNOS) from the plasma membrane to the mitochondria in pulmonary arterial endothelial cells, and that this was dependent on eNOS uncoupling. We also found that ET-1 disturbed carnitine metabolism, resulting in the attenuation of mitochondrial bioenergetics. However, ATP levels were unchanged due to a compensatory increase in glycolysis. Further mechanistic investigations demonstrated that ET-1 mediated the redistribution of eNOS via the phosphorylation of eNOS at Thr495 by protein kinase C ?. In addition, the glycolytic switch appeared to be dependent on mitochondrial-derived reactive oxygen species that led to the activation of hypoxia-inducible factor signaling. Finally, the cell culture data were confirmed in vivo using the monocrotaline rat model of PH. Thus, we conclude that ET-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the redistribution of uncoupled eNOS to the mitochondria, and that preventing this event may be an approach for the treatment of PH. |Adenosine Triphosphate/metabolism [MESH] |Animals [MESH] |Carnitine/metabolism [MESH] |Cell Membrane/metabolism [MESH] |Cells, Cultured [MESH] |Endothelial Cells/*metabolism [MESH] |Endothelin-1/*metabolism [MESH] |Glycolysis/*physiology [MESH] |Mitochondria/*metabolism [MESH] |Nitric Oxide Synthase Type III/*metabolism [MESH] |Phosphorylation [MESH] |Protein Kinase C-delta/metabolism [MESH] |Pulmonary Artery/*metabolism [MESH] |Rats [MESH] |Reactive Oxygen Species/metabolism [MESH]Endothelin-1 induces a glycolytic switch in pulmonary arterial endothe(epmc).pdf DeepDyve Pubget Overpricing