| Literature DB >> 34785240 |
Shuibo Gao1, Haixia Gao1, Liping Dai2, Yongjun Han1, Zhen Lei1, Xinzhou Wang1, Hongbo Chang1, Shanshan Liu1, Zhentao Wang3, Haibin Tong4, Hong Wu5.
Abstract
Promoting angiogenesis by targeting various angiogenic regulators has emerged as a new treatment strategy for myocardial ischemia (MI). MicroRNA-126 (miR-126) has been identified as the main regulator of compensatory angiogenesis; however, its role in MI is unclear. A rat MI model and an EA. hy926 endothelial cell hypoxia model were constructed and it was found that miR-126 was highly expressed in both models. The knockdown of HIF-1α expression in EA. hy926 cells in turn downregulated VEGF and CD34 expression and consequently inhibited angiogenesis. MiR-126 inhibitor inhibited EA. hy926 cell migration and tube formation as well as downregulated VEGF and CD34 expression, and these were reversed by transfection of miR-126 mimics. Rescue tests using miR-126 and HIF-1α demonstrated that miR-126-mediated regulation of angiogenesis was dependent on HIF-1α. In summary, miR-126 regulates the occurrence and progression of angiogenesis during MI via HIF-1α and may be a potential new therapeutic target.Entities:
Keywords: Angiogenesis; HIF-1α; Myocardial ischemia; miR-126
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Year: 2021 PMID: 34785240 DOI: 10.1016/j.yexcr.2021.112925
Source DB: PubMed Journal: Exp Cell Res ISSN: 0014-4827 Impact factor: 3.905