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http://dx.doi.org/10.5483/BMBRep.2017.50.7.085

Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis  

Jo, Ha-neul (Division of Biological Sciences, Sookmyung Women's University)
Kang, Hyesoo (Division of Biological Sciences, Sookmyung Women's University)
Lee, Aram (Division of Biological Sciences, Sookmyung Women's University)
Choi, Jihea (Division of Biological Sciences, Sookmyung Women's University)
Chang, Woochul (Department of Biology Education, College of Education, Pusan National University)
Lee, Myeong-Sok (Division of Biological Sciences, Sookmyung Women's University)
Kim, Jongmin (Division of Biological Sciences, Sookmyung Women's University)
Publication Information
BMB Reports / v.50, no.7, 2017 , pp. 384-389 More about this Journal
Abstract
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.
Keywords
Angiogenesis; Endothelial nitric oxide synthase; MicroRNA-26a; Nogo-B receptor; Vascular endothelial growth factor;
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