Effect of microRNA-10a on expression of brain natriuretic peptide after myocardial ischemia reperfusion in rats
Shaohui Niu, Lihua Zhang, Liguo Jian, Tao Wang
Abstract
Shaohui Niu, Lihua Zhang, Liguo Jian, Tao Wang
Abstract
Objective To investigate the effect of microRNA (miRNA, miR)-10a on the expression of brain natriuretic peptide (BNP) in ventricular remodeling after myocardial ischemia reperfusion injury in rats. Methods Forty-five male Wistar rats were randomly divided into sham operation group A (sham operation group, n=15) and myocardial ischemia reperfusion group (n=30). Rats in myocardial ischemia reperfusion group were inflicted by ligating the left anterior descending coronary of rats. After 24 h, 30 survived rats were randomly divided into group B (myocardial ischemia reperfusion group, n=15) and group C (miR-10a group, n=15). Rats in group C were treated with miR-10a agomirs (80 mg/kg body weight) by tail intravenous injection for 4 weeks, and those in group A and group B were treated with negative control reagents. The expression of histone deacetylase 2 (HDAC2) mRNA was detected by Real-time PCR method respectively. The content of BNP was examined by Western blotting. Results After 4 weeks, the relative expression of HDAC2 mRNA in groups A, B and C was 6.58±0.23×10-5, 14.29±2.16×10-5, and 10.11±1.55×10-5 respectively. Left ventricular mass index was 2.10±0.26, 2.61±0.11, and 2.41±0.12 respectively in groups A, B and C. As compared with group B and group C, the expression of HDAC2 mRNA and BNP in the myocardial ischemia reperfusion zone and left ventricular mass index in group A were significantly increased (P< 0.05). The expression of HDAC2 mRNA and BNP in the myocardial ischemia reperfusion zone and left ventricular mass index in group C were significantly higher than those in group B (P< 0.05). Conclusion miR-10a may improve ventricular remodeling after myocardial ischemia reperfusion in rats via inhibiting the expression of HDAC2 mRNA. Key words: MicroRNA-10a; Histone deacetylase 2; Brain natriuretic peptide; Myocardial ischemia; Reperfusion injury; Myocardial remodeling
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Objective To investigate the effect of microRNA (miRNA, miR)-10a on the expression of brain natriuretic peptide (BNP) in ventricular remodeling after myocardial ischemia reperfusion injury in rats. Methods Forty-five male Wistar rats were randomly divided into sham operation group A (sham operation group, n=15) and myocardial ischemia reperfusion group (n=30). Rats in myocardial ischemia reperfusion group were inflicted by ligating the left anterior descending coronary of rats. After 24 h, 30 survived rats were randomly divided into group B (myocardial ischemia reperfusion group, n=15) and group C (miR-10a group, n=15). Rats in group C were treated with miR-10a agomirs (80 mg/kg body weight) by tail intravenous injection for 4 weeks, and those in group A and group B were treated with negative control reagents. The expression of histone deacetylase 2 (HDAC2) mRNA was detected by Real-time PCR method respectively. The content of BNP was examined by Western blotting. Results After 4 weeks, the relative expression of HDAC2 mRNA in groups A, B and C was 6.58±0.23×10-5, 14.29±2.16×10-5, and 10.11±1.55×10-5 respectively. Left ventricular mass index was 2.10±0.26, 2.61±0.11, and 2.41±0.12 respectively in groups A, B and C. As compared with group B and group C, the expression of HDAC2 mRNA and BNP in the myocardial ischemia reperfusion zone and left ventricular mass index in group A were significantly increased (P< 0.05). The expression of HDAC2 mRNA and BNP in the myocardial ischemia reperfusion zone and left ventricular mass index in group C were significantly higher than those in group B (P< 0.05). Conclusion miR-10a may improve ventricular remodeling after myocardial ischemia reperfusion in rats via inhibiting the expression of HDAC2 mRNA. Key words: MicroRNA-10a; Histone deacetylase 2; Brain natriuretic peptide; Myocardial ischemia; Reperfusion injury; Myocardial remodeling
Key concepts: Ischemia, Medicine, Internal medicine, Brain natriuretic peptide, Group A, Reperfusion injury, Myocardial ischemia, Group B