| Project/Area Number |
06671495
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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) |
NISHIOKA Shigetoshi Kinki University School of Medicine, Department of Orthopaedic Surgery, Associat, 医学部, 助手 (40258033)
松村 文典 近畿大学, 医学部, 助手 (00248014)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | chondrocytes / mechanical stress / protein kinase C / osteoarthritis / 関節軟骨 / メカニカルストレス / 変形性関節症 |
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| Research Abstract |
Although osteoarthritis is one of the popular pathway of joint deterioration results from the mechanical stress loaded on the joint tisse, the underlying mechanism has not been clarified. To elucidate this problem, we introduced Flexercell Strain Unit which enable us to load cyclic tensile stretch on the chondrocytes and investigated the alteration of chondrocytes metabolisms. Cyclic tensile stretch caused morphological change of chondrocytes and enhanced glycosaminoglycan and keratan sulfate release. DNA synthesis was significantly enhanced. On the other hand, cyclic tensile stretch clearly reduced proteoglycan synthesis and inhibitors of protein kinase C reversed stretch-induced inhibition of proteoglycan synthesis. Furthermore, pretreatment of phorbol ester abolished stress-mediated inhibition of proteoglycan synthesis. These data indicate the involvement of protein kinase C in the signal transduction of the mechanical stress loaded on the articular chondrocytes.
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