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Open Access Highly Accessed Research article

Apoptosis is not the major death mechanism induced by celecoxib on rheumatoid arthritis synovial fibroblasts

Rachel Audo1, Véronique Deschamps2, Michael Hahne1, Bernard Combe12 and Jacques Morel12*

Author Affiliations

1 Institut de Génétique Moléculaire de Montpellier, 1919 route de Mende, CNRS UMR5535, Montpellier, France

2 Service d'immuno-rhumatologie et Université Montpellier 1, 371 Ae du doyen Gaston Giraud, Montpellier, France

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Arthritis Research & Therapy 2007, 9:R128  doi:10.1186/ar2342

Published: 12 December 2007

Abstract

Synovial hyperplasia in rheumatoid arthritis (RA) has been associated with apoptosis deficiency of RA fibroblast-like synoviocytes (FLSs). Celecoxib is a non-steroidal anti-inflammatory drug that has been demonstrated to induce apoptosis in some cellular systems. We have therefore examined the dose- and time-dependent effects of celecoxib on RA FLS viability. Treatment of RA FLSs with celecoxib for 24 hours reduced their viability in a dose-dependent manner. Analysis of celecoxib-treated RA FLSs for their content of apoptotic and necrotic cells by Annexin V staining and TO-PRO-3 uptake displayed only few apoptotic cells. Caspase 3, a key mediator of apoptosis, was not activated in celecoxib-treated RA FLSs, and the presence of specific caspase 3 or pan-caspase inhibitors did not affect celecoxib-induced cell death. Moreover, we could not detect other signs of apoptosis, such as cleavage of poly(ADP-ribose) polymerase, caspase 8 or 9, or DNA fragmentation. We therefore conclude that apoptosis is not the major death pathway in celecoxib-treated RA FLSs.