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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)
  • Received : 2017.05.25
  • Accepted : 2017.06.12
  • Published : 2017.07.31

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

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