Apoptosis is not the major death mechanism induced by celecoxib on rheumatoid arthritis synovial fibroblasts
| Autor: | Jacques Morel, Véronique Deschamps, R. Audo, Michael Hahne, Bernard Combe |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
musculoskeletal diseases
Programmed cell death Immunology Arthritis Caspase 3 Apoptosis Caspase 8 Arthritis Rheumatoid TNF-Related Apoptosis-Inducing Ligand Rheumatology Annexin medicine Immunology and Allergy Humans heterocyclic compounds Cyclooxygenase Inhibitors Annexin A5 skin and connective tissue diseases Cells Cultured Cell Proliferation Sulfonamides Cell Death business.industry Anti-Inflammatory Agents Non-Steroidal Synovial Membrane Fibroblasts medicine.disease Staurosporine Celecoxib Cancer research DNA fragmentation Pyrazoles lipids (amino acids peptides and proteins) business medicine.drug Research Article |
| Zdroj: | Arthritis Research & Therapy |
| ISSN: | 1478-6362 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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