Up-regulated expression of microRNA-143 in the adipose tissue of high-fat diet-induced obese mice

Up-regulated expression of microRNA-143 in the adipose tissue of high-fat diet-induced obese mice

Rieko Takanabe1, Koh Ono2, Tomohide Takaya1, Takahiro Horie2, Toru Kita2, Akira Shimatsu1, Koji Hasegawa1.

  1. Division of Translational Research, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan.
  2. Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

第71回日本循環器学会学術集会 (神戸), 2007/03/15 (Featured Research Session).


MicroRNAs (miRNAs) are highly conserved, non-coding RNAs that powerfully regulate gene expression at the post-transcriptional level. Recently, miRNAs have been proposed to play a role in the differentiation of preadipocytes into mature adipocytes in culture. Since changes in gene expression during adipocyte differentiation are closely associated with insulin resistance and cardiovascular diseases, we hypothesized that regulated expression of miRNAs in the adult adipose tissue play a pathophysiological role in obesity in vivo. C57BL/6 mice were fed with either high-fat diet or normal chow. Eight weeks later, severe obesity and insulin resistance was observed in mice on high-fat diet. We measured expression levels of miR-1, miR-24, and miR-143 in mesenteric adipose tissue by real-time PCR. Expression of miR-143 was significantly up-regulated (3-fold) in the adipose tissue on high-fat diet compared to normal chow. However, expression of miR-1 and miR-24 did not differ between high-fat diet and normal chow. One of miR-143 targets is ERK5/BMK1, activation of which has been proposed to inhibit inflammation as well as to promote cell proliferation. Western blot analysis demonstrated that expression of ERK5 in the mesenteric fat tissue was significantly down-regulated expression of miR-143 in the adipose tissue of obese mice, which might contribute to inflammation and adipocyte hypertrophy through down-regulation of ERK5.