Exosomal microRNA-29a mediates cardiac dysfunction and mitochondrial inactivity in obesity-related cardiomyopathy

Endocrine. 2019 Mar;63(3):480-488. doi: 10.1007/s12020-018-1753-7. Epub 2018 Sep 27.

Abstract

Purpose: Present study aims to explore the pathophysiological role of microRNA (miR)-29a in the process of obesity-related cardiomyopathy in human subjects and mice.

Methods: The expression level of circulating exosomal miR-29a was measured in 37 lean and 30 obese human subjects, and correlated with cardiac parameters. The effects of miR-29a on mitochondrial activity and cardiac function were investigated by treatment of miR-29a sponge in primary mouse cardiomyocytes and diet-induced obesity-related cardiomyopathy in mice.

Results: The increased circulating miR-29a level was closely associated with impaired human cardiac function, including ejection fraction (r = -0.2663, p < 0.05) and NT-proBNP levels (r = 0.4270, p < 0.001). Exosomes from obese human plasma mediated cardiomyocyte mitochondrial inactivity, but pre-treatment with miR-29a sponge attenuated the exosomal miR-29a-induced reduction of ATP production (p < 0.001), basal oxygen consumption (p < 0.01) and mitochondrial complex I activity (p < 0.01). In vivo mouse study, high fat diet damaged cardiac function, normal structure, and mitochondrial activity, whereas miR-29a sponge improved the cardiac status.

Conclusions: Present study uncovered the correlation between circulating miR-29a and cardiac parameters in human subjects, and provided solid evidence of the therapeutic application of miR-29a sponge in combating obesity-mediated cardiac dysfunction.

Keywords: Exosome; Heart; MicroRNA-29a; Mitochondria; Obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomyopathies / blood*
  • Cardiomyopathies / etiology
  • Cardiomyopathies / physiopathology
  • Diet, High-Fat / adverse effects
  • Exosomes / metabolism
  • Humans
  • Male
  • Mice, Inbred C57BL
  • MicroRNAs / metabolism*
  • Middle Aged
  • Mitochondria, Heart / metabolism*
  • Natriuretic Peptide, Brain / blood
  • Obesity / blood*
  • Obesity / complications
  • Obesity / physiopathology
  • Peptide Fragments / blood
  • Stroke Volume

Substances

  • MIRN29a microRNA, human
  • MicroRNAs
  • Peptide Fragments
  • pro-brain natriuretic peptide (1-76)
  • Natriuretic Peptide, Brain