miR-126 regulates angiogenesis in myocardial ischemia by targeting HIF-1α

• DOI: 10.1016/j.yexcr.2021.112925
• Publication Date: 2021-11-14T03:19:47Z
• Authors: Shuibo Gao; Haixia Gao; Liping Dai; Yongjun Han; Zhen Lei; Xinzhou Wang; Hongbo Chang; Shanshan Liu; Zhentao Wang; Haibin Tong; Hong Wu
• Keywords: Male; Vascular Endothelial Growth Factor A; 0303 health sciences; Neovascularization, Pathologic; Myocardial Ischemia; Endothelial Cells; Antigens, CD34; Hypoxia-Inducible Factor 1, alpha Subunit; Cell Hypoxia; Rats; 3. Good health; Rats, Sprague-Dawley; MicroRNAs; 03 medical and health sciences; Animals; Humans

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.