| Project/Area Number |
10671366
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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 | Nagasaki University |
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Principal Investigator |
ENOMOTO Hiroshi Nagasaki University School of Medicine, Assistant, 医学部, 助手 (90284679)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Shunichi Nagasaki University School of Medicine, Professor, 医学部, 教授 (30200679)
MATSUMOTO Tomoko Nagasaki University School of Medicine, Associate Professor, 医学部, 助教授 (30239107)
TOMONAGA Tadashi Nagasaki University School of Medicine, Lecturer, 医学部・附属病院, 講師 (00264242)
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| Project Period (FY) |
1998 – 1999
|
| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | chondrocytes / Cartilage tissue / Insulin like growth factor / IGF binding protein / 再生 |
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| Research Abstract |
Insulin-like growth factor-I (IGF-I) is an important anabolic factor for cartilage tissue and its action is in part regulated by IGF-binding proteins (IGFBPs). The object of this study was to investigate the effects of IGFBPs on IGF-I action and on binding of IGF-I to cells using a reproducible immortalized human chondrocyte culture model. Treatment of the C-28/I2 cells with IGF-I or des (1-3 ) IGF-I in serum-free medium stimulated cell proliferation in a dose-dependent manner. However, the effect of des (1-3) IGF-I was more potent, thereby suggesting that endogenously produced IGFBPs inhibited IGF action. The stimulatory effect of IGF-I was inhibited significantly by addition of IGFBP-3. Binding of [125I] IGF-I to the cells was displaced by IGFBP-3. Our findings indicate that the balance between IGFBPs, IGF receptor binding and its action on chondrocyte proliferation may modulate cartilage tissue repair.
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