Using miRNA microarray technology, researchers found that the miR-19a-3p expression level was significantly decreased in the hypertrophic myocardium, and MEF2A was the target gene of miR-19a-3p. The protein expressions of MEF2A, β-MHC, BNP and TRPC1 were significantly increased in hypertrophic cardiomyocytes. MiR-19a-3p was up-regulated after SFI treatment and the protein expressions of these genes were significantly decreased. In addition, miR-19a-3p over-expression in hypertrophic cardiomyocytes could decrease MEF2A mRNA and protein expressions, and anti-miR-19a-3p showed the opposite result.
This study provided substantial evidence that miR-19a-3p plays a functional role in MEF2 signaling in myocardial hypertrophy. SFI attenuated cardiomyocyte hypertrophy probably through up-regulating or maintaining the miR-19a-3p levels and regulating the MEF2 signaling pathway.
Heat map of differentially expressed miRNAs. (A) 13 differentially expressed miRNAs from the myocardial tissues between sham-operation group (n = 3) and model group (n = 3). (B) 10 differentially expressed miRNAs from the myocardial tissues between model group (n = 3) and SFI group (n = 3). Each row represents one miRNA, and each column represents a myocardial tissue sample. The legend on the right indicates miRNA represented in the corresponding row. The relative miRNA expression is depicted according to the color scale. Red indicates up-regulation, and green indicates down-regulation.