| Project/Area Number |
10470372
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Plastic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TAKATO Tsuyoshi Faculty of Medicine, The University of Tokyo, Professor, 医学部・附属病院, 教授 (90171454)
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| Co-Investigator(Kenkyū-buntansha) |
HIKIJI Hisako Faculty of Medicine, The University of Tokyo, Lecturer, 保健管理センター, 講師 (50292876)
SUSAMI Takafumi Faculty of Medicine, The University of Tokyo, Associate Professor, 医学部・附属病院, 助教授 (80179184)
HARII Noriyuki Faculty of Medicine, The University of Tokyo, Professor, 医学部・附属病院, 教授 (50111539)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥11,900,000 (Direct Cost: ¥11,900,000)
Fiscal Year 1999: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1998: ¥8,300,000 (Direct Cost: ¥8,300,000)
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| Keywords | Maxillofacial bone / growth factor / wound healing of bone / 顎顔面 / 下顎骨 / 仮骨延長 / 骨治癒 / 顎整形力 |
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| Research Abstract |
Molecular basis of wound healing of bone affected by mechanical stress has not been studied well. Locally produced autocrine or paracrine factors regulate the wound healing process. Basic fibroblast growth factor (bFGF) has the potent effects on this process. We have shown here the new findings of bFGF.
Fibroblast growth factor-2 (FGF-2) is known to stimulate bone formation and resorption indirectly. We investigated the direct action of on mature osteoclasts. FGF-2 (10-11M) exhibited maximum stimulation (1.9-fold) of pit formation in isolated rabbit osteoclast cultures, whereas in mixed cultures of bone cells, FGF-2 (10-9M) showed the 7.5-fold stimulation. FGF-2 up-regulated the phosphorylation of cellular proteins including p42/p44 mitogen-activated protein (MAP) kinase, and increased the kinase-activity of FGF receptor-1. These results suggest that FGF-2 acts directly on mature osteoclasts through activation of FGF receptor-1 and p42/p44 MAP kinase, causing the stimulation of bone resorption at physiological or pathological concentrations.
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