2006 Fiscal Year Final Research Report Summary
The examination of mucin inducing COX-2 as a pathological molecule of rheumatoid arthritis.
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants |
|Research Institution||Kyoto Prefectural University of Medicine |
KAWAHITO Yutaka Kyoto Prefectural University of Medicine, Graduate School of Medicine, Associate professor -> 京都府立医科大学, 医学研究科, 講師 (50336731)
YOSHIKAWA Toshikazu Kyoto Prefectural University of Medicine, Graduate School of Medicine, Professor, 医学研究科, 教授 (90158410)
TOKUNAGA Daisaku Kyoto Prefectural University of Medicine, School of Medicine, Associate professor, 医学部, 准教授 (90343409)
NAKADA Hiroshi Kyoto Sangyo University, Department of Biotechnology, Faculty of Engineering, Professor, 工学部, 教授 (90113141)
SANO Hajime Hyogo college of medicine, School of Medicine, Professor, 医学部, 教授 (00196304)
|Project Period (FY)
2004 – 2006
|Keywords||mucin inducing COX-2 / rheumatoid arthritis / abnormality of carbohydrate chain|
Abnormality of carbohydrate chain of mucin, which is enriched in synovial fluid (SF), has a possibility to relate with pathological conditions of rheumatoid arthritis (RA) such as the production of IL-1, TNF-a and PGE 2 in joints. In this study, we examine to detect a new mucin as a therapeutic target of RA and analyze its biological activity and structure.
1) Immunohistochemical analysis showed that superficial synovial cells, and infiltrating inflammatory mononuclear cells in RA synovial tissues express MUC-1, Tn and sialyl Tn which are typical malignancy-associated mucins.
2) Western blot analysis revealed that SF faractions purified by gel filtration and further purified preparation by desalination and density-gradient centrifugation include MUC-1, Tn and sialyl Tn.
3) The newly discovered mucin from SF in patients with RA can stimulate the production of IL-1, TNF-a and PGE2 in human peripheral blood monocytes (PBMC).
We revealed that MUC-1, Tn and sialyl Tn expressed in synovial tissues. We also found a new mucin purified from SF in patients with RA, which can produce cytokines and PGE2 on PBMC. This mucin may be mainly MUC-1. We are going to analyze its structure as a therapeutic target of RA and also examine the pathological mechanism including the proliferation of synovial cells and the induction of osteoclast.
Research Products (7 results)