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Trichostatin A sensitises rheumatoid arthritis synovial fibroblasts for TRAIL-induced apoptosis

A Jüngel1, V Baresova, C Ospelt

  • 1Centre of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Gloriastrasse 25, CH 8091 Zurich, Switzerland.

Annals of the Rheumatic Diseases
|November 15, 2005
PubMed
Abstract

Insights

Trichostatin A (TSA) enhances TRAIL-induced apoptosis in rheumatoid arthritis synovial fibroblasts (RASF). This histone deacetylase inhibitor, TSA, sensitizes RASF to TRAIL, suggesting a novel treatment strategy for RA.

Area of Science:

  • Epigenetics and chromatin remodeling
  • Immunology and inflammation
  • Cancer biology and apoptosis

Background:

  • Histone acetylation/deacetylation regulates transcription via chromatin structure modification.
  • Rheumatoid arthritis (RA) involves synovial fibroblasts (RASF).
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis.

Purpose of the Study:

  • To investigate the effect of trichostatin A (TSA) on TRAIL-induced apoptosis in RASF.
  • To analyze TSA's impact on cell proliferation and cell cycle regulators.
  • To assess TRAIL receptor expression and soluble TRAIL levels in RA.

Main Methods:

  • Co-treatment of RASF with TRAIL and TSA.
  • Flow cytometry for apoptosis detection (propidium iodide/annexin-V-FITC).
  • MTS assay for cell proliferation and Western blot for p21Waf1/Cip1.
  • ELISA for soluble TRAIL in synovial fluid.

Main Results:

  • TSA and TRAIL synergistically induced dose-dependent apoptosis in RASF.
  • TSA induced cell cycle arrest via p21Waf1/Cip1 upregulation.
  • Soluble TRAIL levels were higher in RA than osteoarthritis (OA) synovial fluid.

Conclusions:

  • TSA sensitizes RASF to TRAIL-induced apoptosis.
  • TSA may offer a new therapeutic approach for rheumatoid arthritis.
  • TSA targets sensitive sites in the TRAIL signaling pathway.

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