Endothelial miR-26a regulates VEGF-Nogo-B receptor-mediated angiogenesis

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...

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Veröffentlicht in:BMB Reports 2017, 50(7), , pp.384-389
Hauptverfasser: Jo, Ha-Neul, Kang, Hyesoo, Lee, Aram, Choi, Jihea, Chang, Woochul, Lee, Myeong-Sok, Kim, Jongmin
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Sprache:eng
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Zusammenfassung: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. [BMB Reports 2017; 50(7): 384-389]
ISSN:1976-6696
1976-670X
1976-670X
DOI:10.5483/BMBRep.2017.50.7.085