Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1161/CIRCRESAHA.116.304881 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.304881 C4393786!4393786!25722455     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25722455.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Circ+Res 2015 ; 116 (8): 1336-45 Nephropedia Template TP {{tp|p=25722455|t=2015. The Mitochondrial Permeability Transition Pore Regulates Endothelial Bioenergetics and Angiogenesis |pdf=|usr=}}{{25722455}} gab.com Text The Mitochondrial Permeability Transition Pore Regulates Endothelial Bioenergetics and Angiogenesis JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25722455 #FOAvip Rationale: The mitochondrial permeability transition pore (mPTP) is a well-known initiator of cell death that is increasingly recognized as a physiological modulator of cellular metabolism. Objective: We sought to identify how the genetic deletion of a key regulatory subunit of the mPTP, Cyclophilin D (CypD), influenced endothelial metabolism and intracellular signaling. Methods and Results: In cultured primary human endothelial cells (ECs), genetic targeting of CypD using siRNA or shRNA resulted in a constitutive increase in mitochondrial matrix Ca2+ and NADH. Elevated matrix NADH in turn diminished the cytosolic NAD+/NADH ratio and triggered a subsequent downregulation of the NAD+-dependent deacetylase SIRT1. Downstream of SIRT1, CypD-deficient ECs exhibited reduced PTEN expression and a constitutive rise in the phosphorylation of angiogenic Akt. Similar changes in SIRT1, PTEN, and Akt were also noted in the aorta and lungs of CypD KO mice. Functionally, CypD-deficient ECs and aortic tissue from CypD KO mice exhibited a dramatic increase in angiogenesis at baseline and when exposed to vascular endothelial growth factor (VEGF). The NAD+ precursor Nicotinamide mononucleotide restored the cellular NAD+/NADH ratio and normalized the CypD-deficient phenotype. CypD KO mice also presented accelerated wound healing and increased neovascularization upon tissue injury as monitored by optical microangiography (OMAG). Conclusion: Our study reveals the importance of the mPTP in the regulation of endothelial mitochondrial metabolism and vascular function. The mitochondrial regulation of SIRT1 has broad implications in the epigenetic regulation of endothelial phenotype. Twit Text FOAVip The Mitochondrial Permeability Transition Pore Regulates Endothelial Bioenergetics and Angiogenesis ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25722455 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25722455 #FOAvip English Wikipedia <ref>{{Cite pmid|25722455}}</ref> The Mitochondrial Permeability Transition Pore Regulates Endothelial Bioenergetics and Angiogenesis #MMPMID25722455 Marcu R; Kotha S; Zhi Z; Qin W; Neeley CK; Wang RK; Zheng Y; Hawkins BJ Circ Res 2015[Apr]; 116 (8): 1336-45 PMID25722455show ga Rationale: The mitochondrial permeability transition pore (mPTP) is a well-known initiator of cell death that is increasingly recognized as a physiological modulator of cellular metabolism. Objective: We sought to identify how the genetic deletion of a key regulatory subunit of the mPTP, Cyclophilin D (CypD), influenced endothelial metabolism and intracellular signaling. Methods and Results: In cultured primary human endothelial cells (ECs), genetic targeting of CypD using siRNA or shRNA resulted in a constitutive increase in mitochondrial matrix Ca2+ and NADH. Elevated matrix NADH in turn diminished the cytosolic NAD+/NADH ratio and triggered a subsequent downregulation of the NAD+-dependent deacetylase SIRT1. Downstream of SIRT1, CypD-deficient ECs exhibited reduced PTEN expression and a constitutive rise in the phosphorylation of angiogenic Akt. Similar changes in SIRT1, PTEN, and Akt were also noted in the aorta and lungs of CypD KO mice. Functionally, CypD-deficient ECs and aortic tissue from CypD KO mice exhibited a dramatic increase in angiogenesis at baseline and when exposed to vascular endothelial growth factor (VEGF). The NAD+ precursor Nicotinamide mononucleotide restored the cellular NAD+/NADH ratio and normalized the CypD-deficient phenotype. CypD KO mice also presented accelerated wound healing and increased neovascularization upon tissue injury as monitored by optical microangiography (OMAG). Conclusion: Our study reveals the importance of the mPTP in the regulation of endothelial mitochondrial metabolism and vascular function. The mitochondrial regulation of SIRT1 has broad implications in the epigenetic regulation of endothelial phenotype. äThe Mitochondrial Permeability Transition Pore Regulates Endothelial B(epmc).pdf DeepDyve Pubget Overpricing