小鼠心肌肥大 z-bo 2020-12-22 326

　　OBJECTIVE: To use an in vitro model of cardiomyocyte hypertrophy to study the mechanism of miR-133a against cardiomyocyte hypertrophy.

　　Methods: The miR-133a adenovirus expression vector was constructed, introduced into 293 cells, and the virus with high expression of miR-133a was harvested; 12 mouse hearts within 1 to 3 days of birth were taken, and cardiomyocytes were obtained by enzyme digestion and gradient centrifugation. For the control group and the model group, the model group was induced with phenylephrine (PE); the cardiomyocytes of the model group were infected with adenovirus expressing miR-133a, and the changes in cell area were observed. Acta1, Actc1, Actb, Expression of Myh6, Myh7, and BNP genes.

　　Results: After the model group’s cardiomyocytes were cultured with PE, the area was more than 3 times larger than that of the control group, and the expression of Acta1 and other genes were significantly increased. After hypertrophy, the model group’s cardiomyocytes were infected with miR-133a virus than those without miR-133a virus. The area of myocardial cells in the model group was reduced, and the expression of Acta1 and other genes was significantly reduced.

　　Conclusion: miR-133a is an important regulator of myocardial hypertrophy and has the effect of antagonizing myocardial hypertrophy.