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Combinatorial MicroRNAs Suppress Hypoxia-Induced Cardiomyocytes Apoptosis

机译：组合MicroRNA抑制缺氧诱导的心肌细胞凋亡。

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Background/Aims: Our previous in silico analysis revealed potential synergy in the activities of micro(mi)RNAs in myocardial infarction. The present study investigated whether miR-1 and -21 act synergistically to protect against cardiomyocytes apoptosis. Methods: Cell survival was analyzed with cell viability assay; apoptosis was detected by flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labeling, and the caspase-3 activity assay; and protein expression level was determined by western blotting. Results: MiR-1:miR-21 and several other miRNA pairs were evaluated for their potentially synergistic effects against myocardial hypoxia in neonatal rat ventricular cardiomyocytes. Lower combination indices suggested that miRNA pairs acted synergistically to inhibit apoptosis; miR-1 and -21 jointly blocked hypoxia-induced cardiomyocytes apoptosis. Moreover, combined application of miR-1 and -21 activated Akt and blocked hypoxia-induced upregulation of p53 in these cells. Conclusion: MiR-1 and -21 exert synergistic effects against hypoxia-induced cardiomyocytes apoptosis. These results provide a basis for the development of combined miRNA-based therapeutics to treat cardiovascular diseases.
机译：背景/目的：我们先前的计算机分析表明，心肌梗死中的micro（mi）RNA活动具有潜在的协同作用。本研究调查了miR-1和-21是否协同作用来防御心肌细胞凋亡。方法：用细胞活力分析法分析细胞的存活率。流式细胞术，末端脱氧核苷酸转移酶dUTP缺口末端标记和caspase-3活性测定检测细胞凋亡。蛋白质表达水平通过蛋白质印迹法测定。结果：评价了MiR-1：miR-21和其他几对miRNA对新生大鼠心室心肌细胞对心肌缺氧的潜在协同作用。较低的组合指数表明，miRNA对可协同抑制细胞凋亡。 miR-1和-21联合阻断缺氧诱导的心肌细胞凋亡。此外，miR-1和-21的联合应用激活了Akt，并阻止了这些细胞中低氧诱导的p53上调。结论：MiR-1和-21对缺氧诱导的心肌细胞凋亡具有协同作用。这些结果为开发基于miRNA的组合疗法治疗心血管疾病提供了基础。

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