MicroRNA-214在缺氧所致心肌细胞损伤过程中的作用

目的:探讨MicroRNA-214(miR-214)表达的变化与低氧诱导心肌细胞损伤的关系。方法:实时荧光定量PCR技术检测miR-214在心肌细胞低氧损伤中表达的变化。根据培养环境和有无使用miR-214的特异性抑制剂,将心肌细胞分为常氧培养组、常氧培养+miR-214抑制组、低氧培养组及低氧培养+miR-214抑制组。MTT比色法测定各组细胞活力,流式细胞仪(FCM)检测各组细胞的凋亡情况,酶法测定各组细胞的乳酸脱氢酶(LDH)漏出情况。结果:低氧培养后,心肌细胞内的miR-214表达相对常氧培养的对照组有所增高(P0.05),并呈时间依赖关系,低氧培养24 h,miR-214表达相对常氧培养的对照组可增高(1.9±0.1)倍。低氧培养会降低心肌细胞的存活率、增加心肌细胞凋亡及LDH漏出,miR-214抑制后,缺氧造成的上述损伤有所减轻。结论:miR-214的表达水平升高与低氧诱导的心肌细胞损伤有关,可能作为对抗缺氧损伤的靶点和诊断指标。

Role of expression changes of microRNA-214 in injury of cardiomyocytes induced by hypoxia

AIM:To investigate the relationship between cardiomyocyte injury induced by hypoxia and expression of microRNA-214 (miR-214). METHODS: The expression changes of miR-214 mRNA were detected using real- time qPCR technology. Cardiomyocytes were cultured and divided into four groups: normoxia culture group (control), normoxia culture plus miR-214 inhibitor group, hypoxia culture group, and hypoxia culture plus miR-214 inhibitor group. The proliferation of cardiomyocytes in each group was evaluated by MTT assay, apoptosis rate was analyzed by flow cytometry and the lactic dehydrogenase level was measured by enzymatic analysis. RESULTS: After hypoxia culture, a significantly high expression was detected in the cardiomyocytes compared with that in control group. Hypoxia environment inhibited the proliferation of cardiomyocytes, induced apoptosis and increased lactic dehydrogenase level, an injury marker of cardiomyocytes. However, downregulation of miR-214 caused by its specific inhibitor antagonized the cardiomyocyte injury induced by hypoxia. CONCLUSION: High expression of miR-214 is related to cardiomyocyte injury induced by hypoxia and miR-214 may be an underlying target for therapy and potential diagnostic indicator.