Role of miR‐130b/301b cluster in macrophage polarization and obesity

Abstract

Macrophage activation status, such as M1 classic and M2 alternative activation, plays an important role in the development of obesity and other metabolic diseases. The molecular mechanisms regulating macrophage M1/M2 polarization are not fully understood. MicroRNAs are regulatory RNAs that suppress the translation and stability of the mRNA targets. In the present studies, we show that compared to wild type mice, knockout mice of miR‐130b/301b cluster exhibited decreased adiposity, increased whole body energy expenditure, and increased oxygen consumption in response to high fat diet. miR‐130b/301b knockout attenuated the LPS‐induced pro‐inflammatory activation of bone marrow macrophages, while promoted IL‐4 induced alternative macrophage activation. In addition, miR‐130b/301b knockout mice had increased AMP‐activated protein kinase (AMPK) activation in white adipose tissue, which can explain the increased energy expenditure. Together, the present study identified miR‐130b/301b cluster as a novel regulator of macrophage polarization and energy metabolism, which contributes to the development of obesity.Support or Funding InformationThe study is supported by OCAST (PI: Shaoning Jiang) and OK‐INBRE (RPI: Shaoning Jiang) grants.