2018 Fiscal Year Annual Research Report
Fkbp5ノックアウトマウスを用いた不動性・ステロイド性骨粗鬆症発症機構の解明
Project/Area Number |
17J04196
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Research Institution | Nagasaki University |
Principal Investigator |
秦 昕 長崎大学, 医歯薬学総合研究科(歯学系), 特別研究員(DC2)
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Project Period (FY) |
2017-04-26 – 2019-03-31
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Keywords | osteoporosis / Fkbp5 |
Outline of Annual Research Achievements |
To examine the disuse osteoporosis, tail suspension was used for an animal model for unloading. In physiological condition, the bone volume of Fkbp5-/- mice was similar to that of wild-type mice. After tail suspension, bone loss was more severe in Fkbp5-/- mice than wild-type mice in micro-CT analyses. To examine GC-induced osteoporosis, implantation of prednisolone or injection of Dex was performed in wild-type and Fkbp5-/- mice. The GC treatment reduced cortical bone volume and bone formation more severely in Fkbp5-/- mice than wild-type mice. These finding indicated that Fkbp5 inhibits bone loss in unloading and GC treatment.
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Research Progress Status |
平成30年度が最終年度であるため、記入しない。
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Strategy for Future Research Activity |
平成30年度が最終年度であるため、記入しない。
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Research Products
(4 results)