Department of Cardiology, Coal General Hospital, Beijing, China.
Eur Rev Med Pharmacol Sci. 2018 Jan;22(2):532-539. doi: 10.26355/eurrev_201801_14206.
To investigate the role and mechanism of micro ribonucleic acid (miR)-298 in myocardial apoptosis after myocardial infarction.
In vivo experiments, the rat model of myocardial infarction was established, and miR-298 was up-regulated via lentivirus with miR-298 overexpression. Cardiac function of rats was detected via echocardiography, Bcl-2 associated X protein (BAX) expressions in infarction border zone were detected via Real-time Quantitative PCR (qT-PCR) and Western blot, and TUNEL assay was used to detect the myocardial apoptosis. In vitro experiments, myocardial cells were isolated and cultured, an oxygen-glucose deprivation (OGD) model was established to mimicking the ischemic condition, the relationship between miR-298 and BAX was verified using luciferase reporter vector, lentivirus and small-interfering RNA (siRNA) in BAX.
In vivo experiments showed that the miR-298 expression was down-regulated at 2 and 4 weeks after myocardial infarction. The up-regulation of miR-298 significantly improved the cardiac function, decreased the expressions of BAX, reduced the myocardial apoptosis and inhibit the apoptosis proteins expression including cytochrome-c and cleaved caspase-3. In vitro experiments revealed that BAX was a target gene of miR-298 and further proof that miR-298 could inhibit the cytochrome-c and cleaved caspase-3 expression and myocardial apoptosis through BAX.
MiR-298 can improve the myocardial apoptosis through the target gene BAX.
探讨微小核糖核酸（miR）-298 在心肌梗死后心肌细胞凋亡中的作用及机制。
体内实验建立大鼠心肌梗死模型，通过慢病毒过表达 miR-298 上调 miR-298 的表达。通过超声心动图检测大鼠心功能，实时定量聚合酶链反应（qT-PCR）和 Western blot 检测梗死边缘区 Bcl-2 相关 X 蛋白（BAX）的表达，TUNEL 法检测心肌细胞凋亡。体外实验分离培养心肌细胞，建立氧葡萄糖剥夺（OGD）模型模拟缺血状态，通过荧光素酶报告载体、慢病毒和 BAX 的小干扰 RNA（siRNA）验证 miR-298 与 BAX 的关系。
体内实验显示，心肌梗死后 2 周和 4 周时 miR-298 表达下调。miR-298 的上调显著改善了心脏功能，降低了 BAX 的表达，减少了心肌细胞凋亡，并抑制了细胞色素 c 和裂解 caspase-3 的表达。体外实验表明，BAX 是 miR-298 的靶基因，进一步证明 miR-298 可以通过 BAX 抑制细胞色素 c 和裂解 caspase-3 的表达和心肌细胞凋亡。
miR-298 可以通过靶基因 BAX 改善心肌细胞凋亡。
