LAUSR

Objectives: Myocardial cell apoptosis plays a key role in the development of heart failure. Compared with normal myocardial cells, the hypertrophy myocardial cell apoptosis rate increased significantly, as well as their sensitivity to apoptosis stimulating factor, it may be one of the main cause of heart failure. Recent studies have confirmed that mir-139 -3p is involved in the pathological process of tumor occurrence and development. However, it is not clear about the expression and mechanism of mir-139 -3p in cardiac myocytes. In the present study of our team, the increased expression of mir-139 -3p in the myocardial tissue of hypertensive rats was first detected. In this study, we aim to investigate the expression and clinical significance of miR-139-3p in apoptotic cardiomyocytes induced by hypoxia. Methods: The primary neonatal rat cardiomyocytes were cultured. The cardiomyocytes apoptosis model was established by hypoxia. The expression of caspase-3 in apoptosis model was detected by western-blot. The expression of miR-139-3p was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Myocardial cells were observed pseudopod extend, most of cells appear spontaneous rhythmic beat after 48 h cultured. Compared with the normal control group (0.38 + 0.01), the expression of apoptotic protein caspase-3 (1.01 + 0.02) was significantly increased in the experimental group (P < 0.05). The qRT-PCR analysis demonstrated that both apoptotic cardiomyocytes (Hypoxia group) and normal cardiomyocytes (Control group) expressed miR-139-3p. Moreover, relative expression level of miR-139-3p in Hypoxia group (3.25 ± 0.77) was significantly higher than that in Control group (P < 0.05). Conclusion: Expression of miR-139-3p is significantly higher in apoptotic cardiomyocytes than in normal cardiomyocytes, indica