血管生成
生物
基因敲除
调节器
小RNA
治疗性血管生成
转染
癌症研究
川地34
细胞生物学
新生血管
细胞培养
干细胞
基因
生物化学
遗传学
作者
Shuibo Gao,Haixia Gao,Liping Dai,Yongjun Han,Zhen Lei,Wang Xinzhou,Hongbo Chang,Shanshan Liu,Zhentao Wang,Haibin Tong,Hong Wu
标识
DOI:10.1016/j.yexcr.2021.112925
摘要
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.
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