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

Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):9050-9057. doi: 10.26355/eurrev_201910_19307.

Abstract

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.

MeSH terms

  • 3' Untranslated Regions
  • Apoptosis
  • Cell Hypoxia
  • Cell Line
  • Cell Proliferation
  • Humans
  • MicroRNAs / genetics*
  • Models, Biological
  • Myocytes, Cardiac / chemistry
  • Myocytes, Cardiac / cytology*
  • TNF Receptor-Associated Factor 5 / genetics*
  • TNF Receptor-Associated Factor 5 / metabolism

Substances

  • 3' Untranslated Regions
  • MIRN410 microRNA, human
  • MicroRNAs
  • TNF Receptor-Associated Factor 5
  • TRAF5 protein, human