tailieunhanh - Báo cáo khoa học: FLIP and MAPK play crucial roles in the MLN51-mediated hyperproliferation of fibroblast-like synoviocytes in the pathogenesis of rheumatoid arthritis

One of the characteristic features of the pathogenesis of rheumatoid arth-ritis is synovial hyperplasia. We have reported previously that metastatic lymph node 51 (MLN51) and granulocyte–macrophage colony-stimulating factor (GM-CSF) are involved in the proliferation of fibroblast-like synovi-ocytes in the pathogenesis of rheumatoid arthritis. | ễFEBS Journal FLIP and MAPK play crucial roles in the MLN51-mediated hyperproliferation of fibroblast-like synoviocytes in the pathogenesis of rheumatoid arthritis Ju-Eun Ha1 Young-Eun Choi1 Jinah Jang2 Cheol-Hee Yoon1 Ho-Youn Kim3 and Yong-Soo Bae1 2 1 Department of BiologicalScience Sungkyunkwan University Suwon Gyeonggi-do South Korea 2 Division of DC Immunotherapy CreaGene Research Institute Seongnam-shi Gyeonggi-do South Korea 3 Department of Medicine Division of Rheumatology Center for Rheumatoid Diseases and Rheumatism Research Center RhRC Catholic Research Institutes of Medical Sciences Catholic University of Korea Seoul South Korea Keywords FLICE-inhibitory protein granulocytemacrophage colony-stimulating factor metastatic lymph node 51 mitogen-activated protein kinase rheumatoid arthritis fibroblast-like synoviocyte Correspondence . Bae Department of BiologicalScience Sungkyunkwan University 300 Chunchun-dong Jangan-gu Suwon Gyeonggi-do 440-746 South Korea Fax 82 31 290 7087 Tel 82 31 290 5911 E-mail ysbae04@ Received 23 January 2008 revised 5 April 2008 accepted 9 May 2008 One of the characteristic features of the pathogenesis of rheumatoid arthritis is synovial hyperplasia. We have reported previously that metastatic lymph node 51 MLN51 and granulocyte-macrophage colony-stimulating factor GM-CSF are involved in the proliferation of fibroblast-like synoviocytes in the pathogenesis of rheumatoid arthritis. In this study we have found that 1 GM-CSF-mediated MLN51 upregulation is attributable to both transcriptional and post-translational control in rheumatoid arthritis fibroblast-like synoviocytes 2 p38 mitogen-activated protein kinase plays a key role in the upregulation of MLN51 and 3 FLICE-inhibitory protein is upregulated downstream of MLN51 in response to GM-CSF resulting in the proliferation of fibroblast-like synoviocytes. These results imply that GM-CSF signaling activates mitogen-activated protein kinase followed by the upregulation of

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