Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesisopen access
- Authors
- Jo, Ha-neul; Kang, Hyesoo; Lee, Aram; Choi, Jihea; Chang, Woochul; Lee, Myeong-Sok; Kim, Jongmin
- Issue Date
- Jul-2017
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
- Keywords
- Angiogenesis; Endothelial nitric oxide synthase; Micro-RNA-26a; Nogo-B receptor; Vascular endothelial growth factor
- Citation
- BMB REPORTS, v.50, no.7, pp 384 - 389
- Pages
- 6
- Journal Title
- BMB REPORTS
- Volume
- 50
- Number
- 7
- Start Page
- 384
- End Page
- 389
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8254
- DOI
- 10.5483/BMBRep.2017.50.7.085
- ISSN
- 1976-6696
1976-670X
- 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.
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