Effects of myofibrillogenesis regulator on myocardial hypertrophy

AIM: To investigate the effects of myofibrillogenesis regulator-1 (MR1) on myocardial hypertrophy. METHODS: Three stem-loop structures of rMR1 mRNA were selected as targets to establish RNA interference carriers. After transient transfection with plasmids, cultured cardiomyocytes of neonatal were used to perform RT-PCR for choosing the first target to carry out RNA interference blocking MR1 gene. In order to observe the effect of MR1 gene silence on myocardial hypertrophy induced by angiotensin Ⅱ (AngⅡ), the radiation intensity of tritium-leucine ([3H]-Leu) was used to label the cardiomyocytes. Morphological observation, protein extraction and Western blotting were also used to investigate protein synthesis rate, cell surface area and expression of rMR1. RESULTS: The radiation intensity of tritium-Leucine in AngⅡ group increased 21.4% (P0.01), the cell surface area increased 65.8% (P0.01) and the expression of rMR1 was up-regulated. Captopril, an inhibitor of angiotensin converting enzyme, abolished the hypertrophy effect and expression of rMR1 induced by AngⅡ. After MR1 gene blocking, the radiation intensity and cell area decreased 30.2% and 31.1% (P0.01), respectively, compared to AngⅡ group. The expression of rMR1 was depressed. CONCLUSIONS: AngⅡ induces myocardial hypertrophy and upregulates expression of rMR1. Preconditioning with captopril eliminates the effect of AngⅡ, indicating that the increased expression of rMR1 is correlated with myocardial hypertrophy induced by AngⅡ. Blocking of MR1 gene abolishes the effect of AngⅡ and depresseses the expression of rMR1, the effect is similar to ACEI, indicating that MR1 takes part in the procession of hypertrophy through promoting the synthesis of contractive protein in cardiomyocytes.