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Histone deacetylase1 promotes TGF-β1-mediated early chondrogenesis through down-regulating canonical Wnt signaling

Xiaoju Huang1, Jiajia Xu1, Mingjian Huang1

  • 1The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai 200031, China.

Biochemical and Biophysical Research Communications
|December 3, 2014
PubMed

Insights

Histone deacetylase 1 (HDAC1) suppresses Wnt/β-catenin signaling during cartilage formation. This study reveals HDAC1 targets β-catenin gene expression and protein stability, offering a potential therapeutic target for cartilage development.

Area of Science:

  • Biochemistry
  • Developmental Biology
  • Cell Biology

Background:

  • Mesenchymal stem cells (MSCs) differentiation is crucial for cartilage formation in embryonic development and bone repair.
  • Wnt/β-catenin signaling pathway is known to inhibit early chondrogenesis and is downregulated during Transforming growth factor-β1 (TGF-β1)-induced chondrogenesis.

Purpose of the Study:

  • To investigate the mechanisms by which Wnt/β-catenin pathway is downregulated during chondrogenesis.
  • To identify regulatory molecules involved in TGF-β1-induced chondrogenesis.

Main Methods:

  • TGF-β1-induced micromass cultures of C3H10T1/2 cells as a chondrocyte differentiation model.
  • Real-time PCR for gene expression profiling.
  • Luciferase assay, chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and in vitro ubiquitination assays to investigate HDAC1's regulatory role on β-catenin.

Main Results:

  • HDAC1 expression was induced during chondrogenesis.
  • HDAC1 directly suppressed β-catenin gene expression by binding to its promoter.
  • HDAC1 deacetylated β-catenin protein, leading to its degradation.

Conclusions:

  • HDAC1 plays a significant role in regulating chondrogenesis by downregulating Wnt/β-catenin signaling.
  • HDAC1 may serve as a potential therapeutic target for modulating cartilage development and repair.
Keywords:
ChondrogenesisDeacetylationHDAC1TGF-β1Wnt/β-catenin

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