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Published on: December 18, 2019

REST corepressor (CoREST) repression induces phenotypic gene regulation in advanced osteoarthritic chondrocytes

Jun Xiao1, Tao Li, Zhihong Wu

  • 1Department of Orthopaedics and Traumatology, Peking Union Medical College Hospital, PUMC, Beijing, China.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|October 26, 2010
PubMed

Insights

Osteoarthritis progression involves altered chondrocyte phenotype. Researchers found that reduced REST corepressor (CoREST) in osteoarthritis cartilage promotes this change, suggesting CoREST

Area of Science:

  • Biochemistry and Molecular Biology
  • Cell Biology
  • Orthopedics

Background:

  • Osteoarthritis (OA) is characterized by changes in chondrocyte phenotype, including decreased type II collagen and aggrecan, and increased type X collagen.
  • The molecular mechanisms driving these phenotypic alterations in OA remain largely unknown.

Purpose of the Study:

  • To identify key molecules regulating chondrocyte phenotype in osteoarthritis.
  • To investigate the role of REST corepressor (CoREST) in modulating chondrocyte gene expression.

Main Methods:

  • Differential proteomics using two-dimensional gel electrophoresis to compare normal articular cartilage (NAC) and advanced osteoarthritic cartilage (AOC).
  • Protein identification via mass spectrometry.
  • CoREST protein level verification using Western blot.
  • CoREST silencing in NAC chondrocytes using siRNA to assess its effect on chondrocyte-specific gene expression.

Main Results:

  • Nineteen differentially expressed proteins were identified, including CoREST, HHL, and zinc finger protein 155 as potential gene modulators.
  • CoREST protein levels were significantly down-regulated (69.5%) in AOC compared to NAC.
  • CoREST knockdown in NAC chondrocytes led to upregulation of collagen X (a terminal differentiation marker) and downregulation of collagen II and aggrecan (chondrocyte differentiation markers).

Conclusions:

  • Down-regulation of CoREST in osteoarthritic cartilage contributes to the characteristic alterations in chondrocyte phenotype.
  • CoREST plays a homeostatic role in maintaining articular chondrocyte differentiation and function.
  • Targeting CoREST may offer a therapeutic strategy for osteoarthritis.

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