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Ann Rheum Dis 2000;59:143-145 doi:10.1136/ard.59.2.143
  • Concise report

Synovial membrane p53 protein immunoreactivity in rheumatoid arthritis patients

  1. C Soon Leeb,
  2. Ian Porteka,
  3. John Edmondsa,
  4. Bruce Kirkhama
  1. aDepartment of Rheumatology, St George Hospital, University of New South Wales, Australia, bDepartment of Anatomical Pathology, Royal Prince Alfred Hospital, University of Sydney, NSW, Australia
  1. Dr Kirkham and A/Professor Soon Lee, Department of Rheumatology, St George Hospital, Gray Street, Kogarah, New South Wales, Australia 2217
  • Accepted 2 November 1999

Abstract

OBJECTIVES To examine the expression of the p53 protein in synovial membrane of rheumatoid arthritis (RA) patients and to compare this with the expression in normal synovial tissues in subjects without RA.

METHODS Immunohistological expression of the p53 protein was studied using a streptavidin-biotin-peroxidase method and the monoclonal antibody DO-7, an antibody directed against both wild and mutant forms of p53 protein, in synovial tissues of RA patients (n=10) and from subjects with no known joint disease (n=4).

RESULTS p53 protein expression was present in a small percentage of synovial cells in the majority of the RA patients (n=8; 80%) and in half of the normal control cases with no inflammatory joint disease (n=2; 50%). No sample had more than 5% cells staining with intranuclear pattern. The difference in synovial p53 immunoreactivity between the RA patients and normal controls is not statistically significant (p= 0.64; χ2 contingency test).

CONCLUSIONS This study has shown that p53 protein is only weakly expressed in the rheumatoid synovial membrane, with a low percentage of p53 protein immunostaining cells present, with intranuclear staining. These results suggest this is wild type p53 protein rather than mutant protein. These findings suggest that synovial p53 protein expression may not be important in the pathogenesis of RA and may only represent a reactive repair process to DNA damage secondary to the immune and inflammatory reactions associated with the disease.

Footnotes

  • Funding: this project is partly supported by a grant from the Rebecca L Cooper Research Foundation, and the National Health and Medical Research Council of Australia.

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