Growth differentiation factor 11 inhibits adipogenic differentiation by activating TGF-beta/Smad signalling pathway

Hongke Luo1, Yuchen Guo1, Yuting Liu1

  • 1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Cell Proliferation
|May 1, 2019
PubMed
Abstract

Insights

Growth Differentiation Factor 11 (GDF11) inhibits fat cell formation in human mesenchymal stem cells and 3T3-L1 pre-adipocytes. This occurs via the Smad2/3-dependent TGF-beta signaling pathway, impacting adipogenesis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Growth Differentiation Factor 11 (GDF11) is a secreted protein in the TGF-beta superfamily with known roles in development and disease.
  • The specific function of GDF11 in adipogenic differentiation and its underlying molecular mechanisms are not well understood.

Purpose of the Study:

  • To investigate the role of GDF11 in adipogenic differentiation of human mesenchymal stem cells (hMSCs) and 3T3-L1 pre-adipocytes.
  • To elucidate the molecular mechanisms by which GDF11 influences adipogenesis.

Main Methods:

  • hMSCs and 3T3-L1 cells were treated with varying concentrations of recombinant GDF11 (rGDF11) during adipogenic induction.
  • Assays included Oil Red O staining for lipid accumulation, qRT-PCR for gene expression, Western blot, and immunofluorescence staining.

Main Results:

  • rGDF11 demonstrated a dose-dependent inhibition of lipid droplet accumulation in both cell types.
  • Adipogenic gene expression was suppressed by GDF11.
  • GDF11 was found to activate the Smad2/3-dependent TGF-beta signaling pathway, and this inhibition was reversible with a TGF-beta type I receptor inhibitor (SB-431542).

Conclusions:

  • GDF11 significantly inhibits adipogenic differentiation in hMSCs and 3T3-L1 cells.
  • The mechanism involves the activation of the Smad2/3-dependent TGF-beta signaling pathway.

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