2000 Fiscal Year Final Research Report Summary
The mechanism of AP-1 on destruction of bone and cartilage in rheumatoid arthritis.
| Project/Area Number |
11671458
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | JIKEI UNIVERSITY |
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Principal Investigator |
SOSHI Shigeru Jikei University, School of Medicine, Department of Orthopaedic Surgery, Lecturer, 医学部, 講師 (90197012)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Maki Jikei University, School of Medicine, Department of Orthopaedic Surgery, Research Assistant, 医学部, 助手 (00266701)
FUJII Katsuyuki Jikei University, School of Medicine, Department of Orthopaedic Surgery, Professor, 医学部, 教授 (10112856)
TSUJI Michiko Jikei University, School of Medicine, Department of Orthopaedic Surgery, Lecturer, 医学部, 講師 (80207365)
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| Project Period (FY) |
1999 – 2000
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| Keywords | Rheumatoid Arthitis / Activation protein-1 / Bone and cartilage destrcution / Cancellous Condensation |
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| Research Abstract |
Our finding indicate that not only synovial cells but also chondrocytes themselves are potential effector cells for RA cartilage destruction. A normally established balance within the cartilage between matrix proteases and their inhibitors might be alterd during the progression of RA by induction of the expression genes encoding these enzymes. Since the expression level of the c-fos gene is increased in RA chondrocytes, c-fos could be a prime potential candidate for the main pathologic factors in the pathogenesis of RA cartilage destruction. Thus, further studies examining the modulation of c-fos expression may provide an effective approach in preventing joint destruction in RA.
Accordingly, some researches also demonstrated the possibility that some of the mechanisms of anti-inflammatory action glucocorticoids, retinoids, and thiol-binding antirheumatic drugs converge to a final common pathway resulting in inhibition of AP-1 mediated transcription.
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