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BMB Rep. 2017 Jul;50(7):384-389.

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

Author information

1
Division of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
2
Department of Biology Education, College of Education, Pusan National University, Busan 46241, Korea.

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. [BMB Reports 2017; 50(7): 384-389].

PMID:
28602162
PMCID:
PMC5584747
DOI:
10.5483/bmbrep.2017.50.7.085
[Indexed for MEDLINE]
Free PMC Article

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