科研之友
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摘要
Diabetic cardiomyopathy (DCM) is a major complication of diabetes that contributes to the subsequent development of heart failure and increased mortality. Cardiomyocytes apoptosis is considered an important cause for the cardiomyopathy. MicroRNAs have been reported to regulate cell growth, differentiation and cell apoptosis in variety of diseases including cardiovascular disease. However, little is known about the microRNAs regulating cardiomyocytes apoptosis in DCM. We established a rat model of DCM and carried out a microarray to identify the differentially expressed microRNAs in myocardial tissue. Our findings showed that the expression of miR-30b was significantly upregulated in diabetic rats. The present study was designed to investigate the pathogenic role of miR-30b in the development of DCM. To explore the molecular mechanisms involved, we performed in vitro experiments using cultured H9c2 cells. Our results showed that miR-30b expression was associated with high glucose and increased cardiomyocytes apoptosis. Decreased expression of miR-30b by transfecting with miR-30b inhibitor was found to inhibit apoptosis in cardiomyocytes exposed to high glucose. The 3'UTR of Bcl-2 was cloned downstream of a luciferase reporter construct and co-transfected into HEK293 cells with miR-30b mimic. The results of luciferase assay indicated that Bcl-2 might be a direct target of miR-30b. The expression of Bcl-2 was downregulated in cardiomyocytes transfected with miR-30b mimic, which consequently induced cellular apoptosis. In conclusion, our study demonstrates that miR-30b is involved in the regulation of high glucose-induced apoptosis by targeting Bcl-2, which may provide a novel therapeutic strategy for the treatment of DCM.
- 出版日期2017
- 单位山东大学
