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C-myc antisense oligodeoxynucleotides can induce apoptosis and down-regulate Fas expression in rheumatoid

A Hashiramoto1, H Sano, T Maekawa

  • 1Kyoto Prefectural University of Medicine, Japan.

Arthritis and Rheumatism
|May 14, 1999
PubMed
Abstract

Insights

C-myc antisense oligodeoxynucleotides (AS ODN) inhibit rheumatoid arthritis (RA) cell proliferation and induce apoptosis via the caspase cascade. This suggests c-myc AS ODN may be a potential therapeutic for RA.

Area of Science:

  • Molecular Biology
  • Immunology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) pathogenesis involves synovial inflammation and apoptosis.
  • The role of the c-myc oncogene in RA and its impact on synovial apoptosis requires further investigation.

Purpose of the Study:

  • To elucidate the role of c-myc in rheumatoid arthritis (RA) pathogenesis.
  • To investigate the mechanism of synovial apoptosis induced by c-myc modulation.

Main Methods:

  • Utilized cultured human synoviocytes from RA patients.
  • Employed c-myc antisense oligodeoxynucleotides (AS ODN) to inhibit c-myc expression.
  • Assessed cell proliferation (MTT assay), apoptosis (TUNEL staining), Fas expression (flow cytometry, RT-PCR), and caspase cascade involvement (inhibitor assays).

Main Results:

  • c-myc AS ODN treatment inhibited synoviocyte proliferation and down-regulated c-Myc protein and mRNA.
  • Morphological analysis confirmed apoptosis induction.
  • c-myc AS ODN treatment reduced Fas mRNA but not Fas antigen expression.
  • Caspase 1 and caspase 3 inhibitors blocked the cytotoxic effects of c-myc AS ODN.

Conclusions:

  • c-myc AS ODN demonstrates potential as a therapeutic agent for RA.
  • Cell death induced by c-myc AS ODN occurs through the caspase cascade, akin to Fas-induced apoptosis.
  • Combination therapy with anti-Fas antibody and c-myc AS ODN enhanced the reduction of Fas-dependent cytotoxicity.

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