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10.1038/nm.3703 http://scihub22266oqcxt.onion/10.1038/nm.3703 C4257756!4257756!25362254     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Med 2014 ; 20 (12): 1464-71 Nephropedia Template TP {{tp|p=25362254|t=2014. An anti-angiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease |pdf=|usr=}}{{25362254}} gab.com Text An anti-angiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=25362254 #FOAvip Peripheral artery disease (PAD) generates tissue ischemia through arterial occlusions and insufficient collateral vessel formation. Vascular insufficiency in PAD occurs despite higher circulating levels of vascular endothelial growth factor A (VEGF-A),1,2 a key regulator of angiogenesis. Here, we show that clinical PAD is associated with elevated anti-angiogenic VEGF-A splice isoform (VEGF-A165b), and a corresponding reduction of the pro-angiogenic VEGF-A165a isoform. In a murine model of PAD, VEGF-A165b was upregulated by conditions associated with impaired limb revascularization, including leptin-deficiency, diet-induced obesity, genetic ablation of the secreted frizzled-related protein 5 (Sfrp5) adipokine and transgenic overexpression of Wnt5a in myeloid cells. In PAD models, delivery of VEGF-A165b inhibited revascularization of ischemic hind limbs, whereas treatment with an isoform-specific neutralizing antibody reversed the impaired revascularization phenotype caused by metabolic dysfunction or perturbations in the Wnt5a/Sfrp5 regulatory system. These results indicate that inflammation driven expression of the anti-angiogenic VEGF-A isoform can contribute to impaired collateralization in ischemic cardiovascular disease. Twit Text FOAVip An anti-angiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=25362254 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25362254 #FOAvip English Wikipedia <ref>{{Cite pmid|25362254}}</ref> An anti-angiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease #MMPMID25362254 Kikuchi R; Nakamura K; MacLauchlan S; Ngo DTM; Shimizu I; Fuster JJ; Katanasaka Y; Yoshida S; Qiu Y; Yamaguchi TP; Matsushita T; Murohara T; Gokce N; Bates DO; Hamburg NM; Walsh K Nat Med 2014[Dec]; 20 (12): 1464-71 PMID25362254show ga Peripheral artery disease (PAD) generates tissue ischemia through arterial occlusions and insufficient collateral vessel formation. Vascular insufficiency in PAD occurs despite higher circulating levels of vascular endothelial growth factor A (VEGF-A),1,2 a key regulator of angiogenesis. Here, we show that clinical PAD is associated with elevated anti-angiogenic VEGF-A splice isoform (VEGF-A165b), and a corresponding reduction of the pro-angiogenic VEGF-A165a isoform. In a murine model of PAD, VEGF-A165b was upregulated by conditions associated with impaired limb revascularization, including leptin-deficiency, diet-induced obesity, genetic ablation of the secreted frizzled-related protein 5 (Sfrp5) adipokine and transgenic overexpression of Wnt5a in myeloid cells. In PAD models, delivery of VEGF-A165b inhibited revascularization of ischemic hind limbs, whereas treatment with an isoform-specific neutralizing antibody reversed the impaired revascularization phenotype caused by metabolic dysfunction or perturbations in the Wnt5a/Sfrp5 regulatory system. These results indicate that inflammation driven expression of the anti-angiogenic VEGF-A isoform can contribute to impaired collateralization in ischemic cardiovascular disease. äAn anti-angiogenic isoform of VEGF-A contributes to impaired vasculari(epmc).pdf DeepDyve Pubget Overpricing