Tohoku J. Exp. Med., 2023 February, 259(3)

MiR-423-5p Inhibition Exerts Protective Effects on Angiotensin II-Induced Cardiomyocyte Hypertrophy

Meng Xu,1 Dongchen Liu,2 Xinyu Gao,3 Ziwen Wang,1 Linna Zhang1 and Hao Fan1

1Department of Intensive Care Unit, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China
2Department of Coronary Care Unit, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China
3Department of Burn Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China

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

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Tohoku J. Exp. Med 2023, 259, 199-208.

Correspondence: Hao Fan, Department of Intensive Care Unit, The Affiliated Hospital of Xuzhou Medical University, 99 Huaihai West Street, Xuzhou, Jiangsu 221000, China.

e-mail: fanhao12022@163.com