Angiotensin II (Ang II) is a kind of bioactive peptide, which can contribute to cardiac hypertrophy. MicroRNAs (miRNAs) play critical role in various heart diseases. The cardioprotective effect of miR-423-5p inhibition has been confirmed by previous studies. But its role in cardiac hypertrophy induced by Ang II is unknown. This study focused on the potential of miR-423-5p in cardiomyocyte hypertrophy under the treatment of Ang II. Our results revealed that miR-423-5p expression was upregulated in Ang II-treated human cardiomyocytes (HCMs). Importantly, miR-423-5p knockdown suppressed Ang II-induced cardiomyocyte hypertrophy and oxidative stress in HCMs. Bioinformatics analysis and luciferase reporter assay confirmed that the suppressor of Ty 6 homolog (SUPT6H) was a target gene of miR-423-5p. Interestingly, SUPT6H knockdown aggravated cardiomyocyte hypertrophy and oxidative stress in Ang II-stimulated HCMs, which were then reversed by silenced miR-423-5p. In conclusion, miR-423-5p knockdown exerts its protective effects on Ang II-induced cardiomyocyte hypertrophy in HCMs via modulating SUPT6H expression.
Keywords: angiotensin II; cardiomyocyte; heart failure; hypertrophy; miR-423-5p.