Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction
miR-29a regulated the proliferation, migration, and tube formation of cardiac endothelial cells by targeting VEGFA. miR-29a mimics or inhibitors were transfected into cardiac endothelial cells via Lipofectamine 2000; 48 h later, an oxidative stress model was established with the cardiac endothelial cells to investigate the effects of miR-29a. (a) Cell proliferation of cardiac endothelial cells as determined by EdU assays. (b) Quantitative analysis of (a). (c) Migration of cardiac endothelial cells was measured by Transwell migration assays (scale μm). (d) The number of migrated cells per field was determined. (e) Western blot analyses were performed. (f) Relative protein levels of cyclinD1 and PCNA in cardiac endothelial cells were determined. (g) Representative images of cardiac endothelial cells in Matrigel. (h, i) Quantitative assessment of the total number of meshes and branch points. (j) The dual-luciferase activity was verified by cotransfecting either miR-29a mimics or miR-29a-NC and the luciferase reporter vectors pmiRGLO-VEGFA-Mut or pmiRGLO-VEGFA-WT. (k) Relative miR-29a expression in different groups of cardiac endothelial cells was detected via qPCR analysis. (l) VEGFA mRNA expression in cardiac endothelial cells in different groups was also detected by using qPCR analysis. (m) Western immunoblotting was used to detect the relative protein expression of VEGFA. (n) Quantitative analysis of relative VEGFA protein expression (,;, compared with the H2O2 group).
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