1997 Fiscal Year Final Research Report Summary
Role of neuropeptide, substance-p, on the mechanisms of joint destruction in rheumatoid arthritis.
| Project/Area Number |
08671659
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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 | Kobe University |
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Principal Investigator |
SAURA Ryuichi Faculty of Health Science, Kobe University School of Medicine, Associate Professor, 医学部, 助教授 (10252769)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITA Kenji Kobe University Hospital, Assistant, 医学部・附属病院, 助手 (40271043)
MIZUNO Kosaku Kobe University School of Medicine, Professor, 医学部, 教授 (90030981)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Rheumatoid arthritis / Cartilage degradation / Chondrocyte / Neuropeptide / Substance-p / Pain / Cyclooxygenase / Prostaglandin |
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| Research Abstract |
Clinical evidences have suggested that the peripheral nervous system might be involved in the pathophysiology of inflammation. The neuropeptide substance P (SP), which has been found in unmyelinated C fiber of the peripheral sensory nerve, is reported to be one of the possible mediators of chronic inflammation, since it has been detected in inflamed joints and has various biological effects on mesenchymal cells. It is also reported that SP induced collagenase release of synoviocytes obtained from patients with rheumatoid arthritis. However, whether or not SP induces articular cartilage degradation directly, remains unknown. Therefore we have investigated the effect of SP on matrix metalloproteinase release and the accumulation of sulfated glycosaminoglycan of the articular chondrocyte in vitro.
Administration of exogenous SP resulted in the increase of metalloproteinase release in the monolayr cultured bovine articular chondrocytes. Significant increase (p<0.05) was observed at the concentration of 10^<-9> M for 48h incubation. Meanwhile SP had no effect on sulfated glycosaminoglycan synthesis of the articular chondrocyte. These results suggest that SP may increase the deterioration of articular cartilage through augmentation of the release of metalloproteinase in inflammatory arthritis.
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