Concise report
Synovial membrane p53 protein immunoreactivity in rheumatoid
arthritis patients
C Soon Leeb, Ian Porteka, John Edmondsa, Bruce Kirkhama
a Department of
Rheumatology, St George Hospital, University of New South Wales,
Australia, b Department of Anatomical Pathology, Royal Prince
Alfred Hospital, University of Sydney, NSW, Australia
Correspondence to: Dr Kirkham and A/Professor Soon Lee, Department of Rheumatology, St George Hospital, Gray Street, Kogarah, New South Wales, Australia 2217
Accepted for publication 2 November 1999
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;
2 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.
© 2000 by Annals of the Rheumatic Diseases
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