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10.5483/BMBRep.2017.50.7.085 http://scihub22266oqcxt.onion/10.5483/BMBRep.2017.50.7.085 C5584747!5584747!28602162     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMB+Rep 2017 ; 50 (7): 384-9 Nephropedia Template TP {{tp|p=28602162|t=2017. Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis |pdf=|usr=}}{{28602162}} gab.com Text Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis JO: BMB Rep http://www.kidney.de/pget.php?&tw=1&pmid=28602162 #FOAvip The Nogo-B receptor (NgBR) is necessary for not only Nogo-B-mediated angiogenesis but also vascular endothelial growth factor (VEGF)-induced angiogenesis. However, the molecular mechanisms underlying the regulatory role of the VEGF-NgBR axis in angiogenesis are not fully understood. Here, we report that miR-26a serves as a critical regulator of VEGF-mediated angiogenesis through directly targeting NgBR in endothelial cells (ECs). Stimulation of ECs by VEGF increased the expression of NgBR and decreased the expression of miR-26a. In addition, miR-26a decreased the VEGF-induced migration and proliferation of ECs. Moreover, miR-26a overexpression in ECs decreased the VEGF-induced phosphorylation of the endothelial nitric oxide synthase (eNOS) and the production of nitric oxide, which is important for angiogenesis. Overall, these data suggest that miR-26a plays a key role in VEGF-mediated angiogenesis through the modulation of eNOS activity, which is mediated by its ability to regulate NgBR expression by directly targeting the NgBR 3?-UTR. Twit Text FOAVip Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis ????BMB Rep http://www.kidney.de/pget.php?&tw=1&pmid=28602162 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28602162 #FOAvip English Wikipedia <ref>{{Cite pmid|28602162}}</ref> Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis #MMPMID28602162 Jo Hn; Kang H; Lee A; Choi J; Chang W; Lee MS; Kim J BMB Rep 2017[Jul]; 50 (7): 384-9 PMID28602162show ga The Nogo-B receptor (NgBR) is necessary for not only Nogo-B-mediated angiogenesis but also vascular endothelial growth factor (VEGF)-induced angiogenesis. However, the molecular mechanisms underlying the regulatory role of the VEGF-NgBR axis in angiogenesis are not fully understood. Here, we report that miR-26a serves as a critical regulator of VEGF-mediated angiogenesis through directly targeting NgBR in endothelial cells (ECs). Stimulation of ECs by VEGF increased the expression of NgBR and decreased the expression of miR-26a. In addition, miR-26a decreased the VEGF-induced migration and proliferation of ECs. Moreover, miR-26a overexpression in ECs decreased the VEGF-induced phosphorylation of the endothelial nitric oxide synthase (eNOS) and the production of nitric oxide, which is important for angiogenesis. Overall, these data suggest that miR-26a plays a key role in VEGF-mediated angiogenesis through the modulation of eNOS activity, which is mediated by its ability to regulate NgBR expression by directly targeting the NgBR 3?-UTR. äEndothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenes(epmc).pdf DeepDyve Pubget Overpricing