MicroRNA-188 regulates aging-associated metabolic phenotype

Aging Cell. 2020 Jan;19(1):e13077. doi: 10.1111/acel.13077. Epub 2019 Nov 25.

Abstract

With the increasing aging population, aging-associated diseases are becoming epidemic worldwide, including aging-associated metabolic dysfunction. However, the underlying mechanisms are poorly understood. In the present study, we aimed to investigate the role of microRNA miR-188 in the aging-associated metabolic phenotype. The results showed that the expression of miR-188 increased gradually in brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) of mice during aging. MiR-188 knockout mice were resistant to the aging-associated metabolic phenotype and had higher energy expenditure. Meanwhile, adipose tissue-specific miR-188 transgenic mice displayed the opposite phenotype. Mechanistically, we identified the thermogenic-related gene Prdm16 (encoding PR domain containing 16) as the direct target of miR-188. Notably, inhibition of miR-188 expression in BAT and iWAT of aged mice by tail vein injection of antagomiR-188 ameliorated aging-associated metabolic dysfunction significantly. Taken together, our findings suggested that miR-188 plays an important role in the regulation of the aging-associated metabolic phenotype, and targeting miR-188 could be an effective strategy to prevent aging-associated metabolic dysfunction.

Keywords: MicroRNA-188; PRDM16; aging-associated metabolic phenotype; brown adipose tissue; energy expenditure; inguinal white adipose tissue.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging*
  • Animals
  • Humans
  • Male
  • Mice
  • Mice, Knockout
  • MicroRNAs / metabolism*
  • Phenotype
  • Transfection

Substances

  • MIRN188 microRNA, human
  • MicroRNAs