Abstract: Objective To investigate the regulation of miR-1 and miR-133a on L-type calcium channel β2 subunit(Cavβ2) and ??1C subunit during rat cardiomyocyte hypertrophy. Methods Cardiomyocyte hypertrophy was induced by isoproterenol (ISO, 10 ?mol/L). The targets of miR-1 and miR-133a were predicted by online database microCosm and Targetscan, respectively. The 3' untranslated region sequence of Cavβ2 and ?1C were respectively cloned into reporter vector and then transiently transfected into HEK293 cells. The luciferase activities of samples were measured to verify the expression of luciferase reporter vector. The protein expression of Cavβ2 and ?1C were evaluated by Western blot. The expression level of Cavβ2 and ?1C were inhibited by RNAi to determine the effects of Cavβ2 and ?1C on cardiomyocyte hypertrophy. Results 1) Cavβ2 was the one of potential targets of miR-1, ?1C was the one of potential targets of miR-133a. 2) The luciferase activities of HEK293 cells with the plasmid containing widetype Cavβ2 3'UTR sequence or ?1C were significantly decreased when compared with that of control group(P＜0.05, P＜0.01). 3) Upregulation of the miR-1 and miR-133a level by miR-1 mimic and miR-133a mimic transfection could suppress the protein expression of Cavβ2 and ?1C, respectively(P＜0.01, P＜0.05). 4) Downregulation of Cavβ2 and ?1C by RNAi could markedly inhibit the increase of cell surface area(P＜0.01), the mRNA expression of ANP and ?-MHC(P＜0.05). Conclusion Cavβ2 is the target of miR-1, ?1C is the target of miR-133a. MiR-1 and miR-133a can negatively regulate the expression of L-type calcium channel Cavβ2 and ?1C subunit, resulting in the attenuation of cardiomyocyte hypertrophy.

Key words: Key words: microRNA-1, microRNA-133a, L-type calcium channel β2 subunit, L- type calcium channel α1C subunit, cardiomyocyte hypertrophy