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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

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, Korea,
2Department of Biology Education, Pusan National University, Busan, 46241, Korea
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 VEGF-induced migration and proliferation in ECs. Moreover, miR-26a overexpression or NgBR knockdown 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.
Abstract, Accepted Manuscript(in press) [Submitted on May 25, 2017, Accepted on June 12, 2017]
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