Jo Ha-Neul, Kang Hyesoo, Lee Aram, Choi Jihea, Chang Woochul, Lee Myeong-Sok, Kim Jongmin
Division of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Department of Biology Education, College of Education, Pusan National University, Busan 46241, Korea.
BMB Rep. 2017 Jul;50(7):384-389. doi: 10.5483/bmbrep.2017.50.7.085.
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].
Nogo-B受体（NgBR）不仅对Nogo-B介导的血管生成是必需的，而且对血管内皮生长因子（VEGF）诱导的血管生成也是必需的。然而，VEGF-NgBR轴在血管生成中的调节作用的分子机制尚未完全阐明。在此，我们报告miR-26a通过在内皮细胞（ECs）中直接靶向NgBR，作为VEGF介导的血管生成的关键调节因子。VEGF刺激ECs可增加NgBR的表达并降低miR-26a的表达。此外，miR-26a可降低VEGF诱导的ECs迁移和增殖。而且，ECs中miR-26a的过表达可降低VEGF诱导的内皮型一氧化氮合酶（eNOS）磷酸化和一氧化氮的产生，而一氧化氮对血管生成很重要。总体而言，我们的数据表明miR-26a通过调节eNOS活性在VEGF介导的血管生成中起关键作用，这是由其通过直接靶向NgBR 3'-UTR调节NgBR表达的能力介导的。[《BMB报告》2017年；50(7): 384 - 389]
