Overexpression of miRNA-410-3p protects hypoxia-induced cardiomyocyte injury via targeting TRAF5

Y.-L. Teng, F. Ren, H. Xu, H.-J. Song

Department of Cardiac Function Room, The First People’s Hospital of Lianyungang (Xuzhou Medical University Affiliated Hospital of Lianyungang), Lianyungang, China. hjsong660758@163.com

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• Cardiology

OBJECTIVE: This study aims to clarify the influence of microRNA-410-3p (miRNA-410-3p) on hypoxia-induced injury in cardiomyocytes.

MATERIALS AND METHODS: MiRNA-410-3p level, apoptotic rate, and cell viability in AC16 cells undergoing normoxia or hypoxia preconditioning were assessed. The regulatory effects of miRNA-410-3p and TRAF5 on the proliferative and apoptotic abilities of AC16 cells were evaluated. The binding relationship between miRNA-410-3p and TRAF5 was verified by Dual-Luciferase Reporter Gene Assay.

RESULTS: Hypoxia preconditioning triggered apoptosis and inhibited the viability in AC16 cells. MiRNA-410-3p was downregulated in cardiomyocytes under the hypoxic environment. The overexpression of miRNA-410-3p stimulated proliferation and inhibited apoptosis in hypoxia preconditioning AC16 cells. TRAF5 was proved to be the target of miRNA-410-3p. TRAF5 level was negatively regulated by miRNA-410-3p. The silence of TRAF5 could reverse viability and apoptosis changes in hypoxic AC16 cells overexpressing miRNA-410-3p.

CONCLUSIONS: MiRNA-410-3p protects hypoxia-induced proliferation suppression and apoptosis stimulation in cardiomyocytes via targeting TRAF5.

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