BMP-TAK1 (MAP3K7) Induces Adipocyte Differentiation Through PPARγ Signaling

Yongchun Zhang, Regis J. O'Keefe, Jennifer H. Jonason

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

BMPs have been shown to promote adipocyte differentiation through SMAD-dependent signaling. However, the role of TGF-β-activated kinase 1 (TAK1) in non-canonical BMP signaling in adipocyte differentiation remains unclear. Here, we show that TAK1 inhibition decreases lipid accumulation in C3H10T1/2 mesenchymal stem cells (MSCs) induced to differentiate into adipocytes. TAK1 knockdown by siRNA further confirms that TAK1 is required for adipocyte commitment of MSCs. Additionally, TAK1 knockdown inhibits adipogenesis of 3T3-L1 preadipocytes, indicating that TAK1 is not only needed for adipocyte commitment, but also required for adipocyte terminal differentiation. Furthermore, TAK1 ablation specifically in adipocytes reduced high fat diet-induced weight gain and improved glucose tolerance. Mechanistically, we demonstrate that TAK1 is required for PPARγ transactivation and promotes PPARγ transcriptional activity synergistically with TAK1 binding protein 1 (TAB1). Collectively, our results demonstrate that TAK1 plays a critical role in BMP-mediated adipocyte differentiation. J. Cell. Biochem. 118: 204–210, 2017.

Original languageEnglish
Pages (from-to)204-210
Number of pages7
JournalJournal of cellular biochemistry
Volume118
Issue number1
DOIs
StatePublished - Jan 1 2017

Keywords

  • ADIPOCYTE
  • BMP
  • OBESITY
  • PPARγ
  • TAK1

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