| Project/Area Number |
08671699
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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 | Kinki University |
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Principal Investigator |
FUKUDA Kanji Kinki University School of Medicine, Department of Orthopaedic Surgery, Lecturer, 医学部, 講師 (50201744)
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| Co-Investigator(Kenkyū-buntansha) |
OOTANI Kazuhiro Kinki University School of Medicine, Department of Orthopaedic Surgery, Associat, 医学部, 助手 (20258031)
松村 文典 近畿大学, 医学部, 助手 (00248014)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | chondrocytes / mechanical stress / nitric oxide / osteoarthritis / protein kinase C / 機械的ストレス / プロテオグリカン |
|---|
| Research Abstract |
Osteoarthrosis, a common pathway of joint deterioration, is caused by mechanical stress loaded on articular cartilage. We previously demonstrated the involvement of protein kinase C in the development of osteoarthritis in vitro. In the present study, we examined the effect of mechanical stress on chondrocyte metabolism and the activity of protein kinase C in vitro. Low frequency and magnitude of cyclic tensile stretch loaded on chondrocytes increased proteoglycan synthesis. However, high frequency and magnitude of stress decreased its synthesis. In this condition, activity of protein kinase C was reduced. These results suggest an involvement of protein kinase C in the stress mediated inhibition of proteoglycan synthesis. We also investigated the alteration of nitric oxide with mechanical stress. Both conditions caused the inhibition of No synthesis, thereby indicating the involvement of No in stress mediated alteration of the chondrocyte metabolism.
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