科研之友
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摘要
Background and aim: Previous findings have indicated that abnormal expression level of microRNA in endothelial progenitor cells (EPCs) is correlated with dysfunction of EPCs. EPCs have a beneficial effect on endothelial repair and integrity which fight against coronary artery disease (CAD). This study aimed to determine the role that microRNA-222 plays on human EPC functions and investigate the underlying mechanisms. Methods: EPCs were separately collected from peripheral blood mononuclear cells of patients with CAD and healthy donors. EPC functions (proliferation, adhesion and migration) were performed by CCK-8 assay, cell counting, and Transwell migration assay. Identification of the target gene of miR-222 was studied by bioinformatics and Western blot analysis. Expression of miR-222 was measured by quantitative real-time polymerase chain reaction. Protein levels were analyzed by Western blot. Furthermore, vascular endothelial growth factor (VEGF) production was quantified by enzyme-linked immunosorbent assay. Results: miR-222 was significantly higher in CAD EPCs than in healthy donor-derived EPCs. Overexpression of miR-222 in healthy donor-derived EPCs contributed to decreases in proliferation, adhesion, and migration in vitro. Conversely, downregulation of miR-222 effectively reverted CAD EPC functions. STAT5A is a target of miR-222 in EPCs. The overexpression or inhibitory level of miR-222 regulated VEGF production and p38 mitogen-activated protein kinase (MAPK) activation in human EPCs. Conclusions: Downregulation of miR-222 might facilitate CAD EPC function through the activation of p38 MAPK/VEGF signal pathway. Thus, inhibition of miR-222 might have important medical applications in EPC-based therapy for CAD.
- 出版日期2018
- 单位江苏大学
