tailieunhanh - Báo cáo y học: " MAPK signalling in rheumatoid joint destruction: can we unravel the puzzle? "

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: MAPK signalling in rheumatoid joint destruction: can we unravel the puzzle? | Available online http content 7 5 177 Commentary MAPK signalling in rheumatoid joint destruction can we unravel the puzzle Lars-Henrik Meyer and Thomas Pap Division of Molecular Medicine of Musculoskeletal Tissue Department of Orthopaedics University Hospital of Munster Munster Germany Corresponding author Thomas Pap Published 16 August 2005 Arthritis Research Therapy 2005 7 177-178 DOI ar1810 This article is online at http content 7 5 177 2005 BioMed Central Ltd See related research by Goertz et al. in this issue http content 7 5 R1140 Abstract Mitogen-activated protein kinases MAPKs have been associated with the pathogenesis of rheumatoid arthritis RA but the individual contributions of the three MAPK family members are incompletely understood. Although previous data have established a role for c-Jun N-terminal kinase JNK and extracellular signal-related kinase ERK in different animal models of arthritis most recent data indicate that the stable activation of p38 MAPK and in part of ERK significantly contributes to destructive arthritis in mice transgenic for human tumour necrosis factor-a. These data highlight the complexity of MAPK signalling in arthritis and provide a basis for the design of novel strategies to treat human RA. Although all three mitogen-activated protein kinase MAPK families - p38 extracellular signal-related kinase ERK and c-Jun N-terminal kinase JNK - seem to be involved in the activation of synovial cells in rheumatoid arthritis RA the main pathways involved in the regulation of joint destruction are incompletely understood. In this issue of Arthritis Research Therapy Goertz and colleagues report some important novel data on MAPK activation in arthritic mice transgenic for human tumour necrosis factor-a hTNFtg mice 1 . With the use of Western blotting and immunohistochemistry they show that p38 MAPK and ERK are the primarily activated .