| Project/Area Number |
12671426
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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 | Kumamoto University |
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Principal Investigator |
MIZUTA Hiroshi Kumamoto University, School of medicine, Assistant professor, 医学部, 助教授 (60174025)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Eiichi Kumamoto University, School of medicine, Assistant, 医学部附属病院, 助手 (70274719)
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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 |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | fibroblast growth factor / full-thickness defect / repair / mesenchymal stem cell / cell migration / chondrogenesis / fibroblast growth factor2 / clearance / chemotaxis / fibroblast growth factor-2 / PCNA / short term treatment |
|---|
| Research Abstract |
We investigated the effect of shorter exposure of fibroblast growth factor (FGF)-2 on the repair of die fufl-thickness defects of articular cartilage of rabbits. Five-mm full-thickness articular cartilage defects, which are not repaired spontaneously, were created in the femoral trochlea, and FGF-2 (150 pg/h) was administered into the joint cavity with an osmotic delivery system for 1 day, 3 days, 1 week or 2 weeks. By the treatment with FGF-2 for only 1 day, the defects were resurfaced wife cartilaginous matrix as successfully as those treated for 2 weeks. Immunohistochemical analyses using anti-proliferating cell nuclear antigen demonstrated high proliferative activity of mesenchymal cells in the reparative tissues at 1 week in all FGF-2 treated groups. Clearance of FGF-2 administered into the defect was monitored by a radiotope study. Half-life of FGF-2 in the defect cavity was estimated to be 【less than or equal】 30 min. We also examined in vitro the FGF-2 action on the migration of rabbit marrow-derived mesenchymal cells and found a chemotactic response of those cells to FGF-2. These results indicate that FGF-2 signals participate in mobilization and recruitment of actively replicating mesenchymal cells from bone marrow into the defect cavities.
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