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(American Journal of Pathology. 2002;160:123-130.)
© 2002 American Society for Investigative Pathology

Regular Articles

Regulation of Joint Destruction and Inflammation by p53 in Collagen-Induced Arthritis

Yuji Yamanishi*, David L. Boyle*, Michael J. Pinkoski{dagger}, Artin Mahboubi{dagger}, Tesu Lin{dagger}, Zuoning Han*, Nathan J. Zvaifler*, Douglas R. Green{dagger} and Gary S. Firestein*

From the University of California at San Diego School of Medicine,*
La Jolla; and the La Jolla Institute of Allergy and Immunology,{dagger}
La Jolla, California

The role of the tumor suppressor p53 as a key regulator of inflammation was examined in murine collagen-induced arthritis (CIA), a model of rheumatoid arthritis. Wild-type DBA/1 mice develop progressive arthritis in this model, in which p53 expression and apoptosis are evident in the synovial cells. In contrast, the joints of p53-/- DBA/1 animals with CIA showed increased severity of arthritis using clinical and histological scoring methods with almost no apoptosis. Consistent with this, collagenase-3 expression and cytokine production (interleukin-1 and interleukin-6) in the joints of p53-/- mice with CIA were significantly greater than in wild-type mice. Anti-collagen antibody titers, however, were not different. Therefore, p53 expression occurs during inflammation and acts to suppress local inflammatory responses. Because mutations in p53 have been described in the synovial membrane of rheumatoid arthritis patients, the loss of p53 function in synoviocytes or other cells in the joint because of dominant-negative mutations might contribute to invasion and destruction of the joint in this disease.




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