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: Chondrocyte response to growth factors is modulated by p38 mitogen-activated protein kinase inhibition. | Arthritis Research Therapy Vol 6 No 1 Studer et al. Research article Open Access Chondrocyte response to growth factors is modulated by p38 mitogen-activated protein kinase inhibition Rebecca K Studer Rachel Bergman Tiffany Stubbs and Kimberly Decker VA Pittsburgh Healthcare System University of Pittsburgh Medical School Department of Orthopaedic Surgery Pittsburgh Pennsylvania USA Correspondence Rebecca K Studer e-mail rstuder@ Received 24 Jul 2003 Revisions requested 16 Sep 2003 Revisions received 23 Sep 2003 Accepted 16 Oct 2003 Published 7 Nov 2003 Arthritis Res Ther 2004 6 R56-R64 DOI ar1022 2004 Studer et al. licensee BioMed Central Ltd Print ISSN 1478-6354 Online ISSN 1478-6362 . This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Inhibitors of p38 mitogen-activated protein kinase MAPK diminish inflammatory arthritis in experimental animals. This may be effected by diminishing the production of inflammatory mediators but this kinase is also part of the IL-1 signal pathway in articular chondrocytes. We determined the effect of p38 MAPK inhibition on proliferative and synthetic responses of lapine chondrocytes cartilage and synovial fibroblasts under basal and IL-1-activated conditions. Basal and growth factor-stimulated proliferation and proteoglycan synthesis were determined in primary cultures of rabbit articular chondrocytes first-passage synovial fibroblasts and cartilage organ cultures. Studies were performed with or without p38 MAPK inhibitors in IL-1-activated and control cultures. Media nitric oxide and prostaglandin E2 were assayed. p38 MAPK inhibitors blunt chondrocyte and cartilage proteoglycan synthesis in response to transforming growth factor beta responses to insulin-like growth factor 1 IGF-1 and fetal calf serum FCS are unaffected. p38 MAPK inhibitors significantly reverse
