miR-8485 alleviates the injury of cardiomyocytes through TP53INP1

J Biochem Mol Toxicol. 2022 Oct;36(10):e23159. doi: 10.1002/jbt.23159. Epub 2022 Jul 25.

Abstract

MicroRNAs (miRNAs) feature prominently in regulating the progression of chronic heart failure (CHF). This study was performed to investigate the role of miR-8485 in the injury of cardiomyocytes and CHF. It was found that miR-8485 level was markedly reduced in the plasma of CHF patients, compared with the healthy controls. H2 O2 treatment increased tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels, inhibited the viability of human adult ventricular cardiomyocyte cell line AC16, and increased the apoptosis, while miR-8485 overexpression reversed these effects. Tumor protein p53 inducible nuclear protein 1 (TP53INP1) was identified as a downstream target of miR-8485, and TP53INP1 overexpression weakened the effects of miR-8485 on cell viability, apoptosis, as well as inflammatory responses. Our data suggest that miR-8485 attenuates the injury of cardiomyocytes by targeting TP53INP1, suggesting it is a protective factor against CHF.

Keywords: TP53INP1; cardiomyocytes; chronic heart failure; miR-8485.

MeSH terms

  • Apoptosis
  • Carrier Proteins* / genetics
  • Carrier Proteins* / metabolism
  • Heat-Shock Proteins* / genetics
  • Heat-Shock Proteins* / metabolism
  • Humans
  • Interleukins / metabolism
  • Interleukins / pharmacology
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Myocytes, Cardiac* / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Carrier Proteins
  • Heat-Shock Proteins
  • Interleukins
  • MIRN8485 microRNA, human
  • MicroRNAs
  • TP53INP1 protein, human
  • Tumor Necrosis Factor-alpha
  • Tumor Suppressor Protein p53