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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: Rheumatoid arthritis as a hyper-endoplasmic reticulumassociated degradation disease. | Available online http arthritis-research.eom content 7 5 181 Commentary Rheumatoid arthritis as a hyper-endoplasmic reticulum-associated degradation disease Satoshi Yamasaki1 Naoko Yagishita1 Kaneyuki Tsuchimochi1 Kusuki Nishioka2 and Toshihiro Nakajima1 1 Department of Genome Science Institute of Medical Science St Marianna University School of Medicine Kawasaki Kanagawa Japan 2Rheumatology Immunology and Genetics Program Institute of Medical Science St Marianna University School of Medicine Kawasaki Kanagawa Japan Corresponding author Toshihiro Nakajima nakashit@marianna-u.ac.jp Published 17 August 2005 This article is online at http arthritis-research.com content 7 5 181 2005 BioMed Central Ltd Arthritis Research Therapy 2005 7 181-186 DOI 10.1186 ar1808 Abstract We introduce Synoviolin as a novel pathogenic factor in rheumatoid arthritis RA . Experimental studies indicate that this endoplasmic reticulum ER -resident E3 ubiquitin ligase has important functions in the ER-associated degradation ERAD system an essential system for ER homeostasis. Overexpression of Synoviolin in mice causes arthropathy with synovial hyperplasia whereas heterozygous knockdown results in increased apoptosis of synovial cells and resistance to collagen-induced arthritis in mice. On the basis of these experimental data we propose that excess elimination of unfolded proteins that is hyper-ERAD by overexpression of Synoviolin triggers synovial cell overgrowth and hence a worsening of RA. Further analysis of the hyper-ERAD system may permit the complex pathomechanisms of RA to be uncovered. Introduction There is a general agreement that synovial cells have a crucial function in rheumatoid arthritis RA by forming a mass of synovial tissue which promotes the production of matrixdegrading proteases and osteoclast activation that lead to joint destruction 1-6 . In a series of experiments that focused on synovial cells we determined that human T cell leukemia virus type I HTLV-I causes .
