| Project/Area Number |
12470303
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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 |
Orthopaedic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KAWAGUCHI Hiroshi Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (40282660)
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Nobuyuki Kyoto University, Department of Genetic Biochemistry, Professor, 大学院・薬学系, 教授 (10110610)
NAKAMURA Kozo Faculty of Medicine, Professor, 医学部附属病院, 教授 (60126133)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,600,000 (Direct Cost: ¥14,600,000)
Fiscal Year 2002: ¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2000: ¥7,100,000 (Direct Cost: ¥7,100,000)
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| Keywords | fibroblast growth factor (FGF) / bone / cartilage / osteoblasts / osteoclast / chondrocyte / growth factor / 下皮骨細胞 |
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| Research Abstract |
This study investigated the actions of FGF-18, a novel member of the FGF family on osteoblasts, chondrocytes and osteoclasts, and compared them with those of FGF-2 and FGF-10. FGF-18 stimulated the proliferation of cultured mouse primary osteoblasts, osteoblastic cell line MC3T3-E1 cells, primary chondrocytes and prechondrocytic cell line ATDC5 cells, although it inhibited the differentiation and matrix synthesis of these cells. FGF-18 up-regulated the phosphorylation of extracellular signal-regulated kinase (ERK) both in osteoblasts and chondrocytes, and p38 mitogen-activated protein kinase (MAPK) only in chondrocytes. FGF-18 mitogenic actions were blocked by a specific inhibitor of ERK in both cells, and by that of p38 MAPK in chondrocytes. Regarding the action of FGF-18 on bone resorption, FGF-18 not only induced osteoclast formation through receptor activator of NF-κB ligand and cyclooxygenase-2, but also stimulated osteoclast function to form resorbed pits on a dentine slice in the mouse coculture system. All these effects of FGF-18 bore a close resemblance to those of FGF-2, whereas FGF-10 affects none of these cells. FGF-18 may therefore compensate the action of FGF-2 on bone and cartilage.
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