Q Zhang1, N Yu, B-T Yu. 1. Department of Cardiology, Coal General Hospital, Beijing, China. fengyeqiqi9999@163.com.
Abstract
OBJECTIVE: To investigate the role and mechanism of micro ribonucleic acid (miR)-298 in myocardial apoptosis after myocardial infarction. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: MiR-298 can improve the myocardial apoptosis through the target gene BAX.
OBJECTIVE: To investigate the role and mechanism of micro ribonucleic acid (miR)-298 in myocardial apoptosis after myocardial infarction. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS:MiR-298 can improve the myocardial apoptosis through the target gene BAX.