BMB Reports 2017; 50(7): 384-389  https://doi.org/10.5483/BMBRep.2017.50.7.085
Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis
Ha-neul Jo1,#, Hyesoo Kang1,#, Aram Lee1, Jihea Choi1, Woochul Chang2, Myeong-Sok Lee1 & Jongmin Kim1,*
1Division of Biological Sciences, Sookmyung Women’s University, Seoul 04310, 2Department of Biology Education, College of Education, Pusan National University, Busan 46241, Korea
Correspondence to: Tel: +82-2-710-9553; Fax: +82-2-2077-7322; E-mail: jkim@sookmyung.ac.kr
#These authors contributed equally to this work.
Received: May 25, 2017; Revised: June 8, 2017; Accepted: June 12, 2017; Published online: July 31, 2017.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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, our 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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