BMP and activin membrane-bound inhibitor (BAMBI) inhibits the adipogenesis of porcine preadipocytes through Wnt/β-catenin signaling pathway

Abstract

The process of differentiation from preadipocytes to adipocytes contributes to adipose tissue expansion in obesity. Blocking adipogenesis may be conducive to the etiology of obesity-related diseases. BMP and activin membrane-bound inhibitor (BAMBI) is a transmembrane protein, which was identified as a target of β-catenin in colorectal and hepatocellular tumor cells. However, whether BAMBI affects adipogenesis by Wnt/β-catenin signaling remains to be explored. In this study, we distinguish BAMBI as an inhibitor of preadipocytes differentiation. We found that BAMBI was downregulated during preadipocytes differentiation. Knockdown of BAMBI increased adipogenesis and blocked Wnt/β-catenin signaling by repressing β-catenin accumulation. In BAMBI overexpression cells, lipid accumulation was reduced by promoting nuclear translocation of β-catenin. Lithium chloride (LiCl) is an activator of Wnt/β-catenin signaling, which is an inhibitor of glycogen synthetase kinase-3 (GSK-3), maintaining the stability of β-catenin in cytosolic. We showed BAMBI strengthened the anti-adipogenic effects of LiCl. In addition, the results indicated that BAMBI was upregulated by β-catenin. These observations illuminated that BAMBI inhibits adipogenesis by a feedback loop (BAMBI→β-catenin nuclear translocation→BAMBI), which forms with Wnt/β-catenin signaling.