内皮细胞微小RNA-26a调控血管内皮生长因子-轴突生长抑制因子B受体介导的血管生成。
Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis.
作者信息
Jo Ha-Neul, Kang Hyesoo, Lee Aram, Choi Jihea, Chang Woochul, Lee Myeong-Sok, Kim Jongmin
机构信息
Division of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Department of Biology Education, College of Education, Pusan National University, Busan 46241, Korea.
出版信息
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]
Zotero 插件