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Báo cáo y học: CD95-induced osteoarthritic chondrocyte apoptosis and necrosis: dependency on p38 mitogen-activated protein kinase

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: CD95-induced osteoarthritic chondrocyte apoptosis and necrosis: dependency on p38 mitogen-activated protein kinase. | Available online http arthritis-research.eom content 8 2 R37 Research article CD95-induced osteoarthritic chondrocyte apoptosis and necrosis dependency on p38 mitogen-activated protein kinase Lei Wei Xiao-juan Sun Zhengke Wang and Qian Chen Department of Orthopaedics Brown Medical School Rhode Island Hospital Providence Rhode Island USA Corresponding author Lei Wei lwei@lifespan.org Received 20 Jun 2005 Revisions requested 14 Jul 2005 Revisions received 12 Dec 2005 Accepted 19 Dec 2005 Published 16 Jan 2006 Arthritis Research Therapy 2006 8 R37 doi 10.1186 ar1 891 This article is online at http arthritis-research.com content 8 2 R37 2006 Wei et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract One of the hallmarks of osteoarthritic cartilage is the loss of chondrocyte cellularity due to cell death. However considerable controversy has recently arisen surrounding the extent of apoptotic cell death involved in development of osteoarthritis OA . To shed light on this issue we characterized cell death in primary OA chondrocytes mediated by the CD95 Fas pathway. Treatment of chondrocytes with anti-CD95 not only increased the rate of cell death but also increased the production of CD95 ligand by chondrocytes. This reveals a novel autocrine regulatory loop whereby activated chondrocytes may amplify CD95 signals by inducing synthesis of CD95 ligand. Multiple morphologic detection analyses indicated that apoptosis accounted for only a portion of chondrocyte death whereas the other chondrocytes died by necrosis. Both chondrocyte apoptosis and necrosis depended on the activity of p38 mitogen-activated protein kinase MAPK within chondrocytes. Treatment of chondrocytes with the p38 MAPK inhibitor SB203580 .