| Project/Area Number |
22591698
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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 | Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology |
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Principal Investigator |
TOKIMURA Fumiaki 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (80242147)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAZAKI Tsuyoshi 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (50376480)
TANAKA Sakae 東京大学, 医学部附属病院・整形外科, 教授 (50282661)
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Sakae 東京大学, 医学部附属病院・整形外科, 教授 (50282661)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨関節破壊 / 破骨細胞 / ミトコンドリア / 骨吸収 / 関節リウマチ |
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| Research Abstract |
To explore the relationship between osteoclastic bone resorption and mitochondrial morphology, we constructed adenoviruses carrying wild type Drp1 or dominant negative form of Drp1 (Drp1K38A, a point mutation at Lys-38 to Ala). Infection of AxDrp1K38A did not have any effect on osteoclast survival. However, the expression of Drp1K38A caused cytoskeletal disorganization of osteoclasts and suppressed pit-forming activity of the cells in vitro. These results suggest a potential application of mitochondrial fission to control osteoclastic bone resorption.
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