| Project/Area Number |
26670811
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional basic dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
KOMORI Toshihisa 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (00252677)
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| Co-Investigator(Renkei-kenkyūsha) |
MORIISHI Takeshi 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (20380983)
FUKUYAMA Ryo 広島国際大学, 薬学部, 講師 (20389117)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | グルココルチコイド / ステロイド性骨粗鬆症 / Fkbp5 / 骨細胞 / メカルカルストレス / 骨粗鬆症 / Bcl2 / 非荷重 |
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| Outline of Final Research Achievements |
We are clarifying the functions of osteocyte network using osteoblast-specific Bcl2 transgenic mice, in which osteocyte network is completely disrupted. We identified Fk506 binding protein 5 (Fkbp5), which was induced in osteoblasts and osteocytes on unloaded condition in the presence of osteocyte network.
Fkbp5 is a chaperon molecule, which binds to steroid receptor. To investigate the functions of Fkbp5 in bone, we generated Fkbp5 knockout (Fkbp5-/-) mice. Fkbp5-/- mice showed more severe reductions of bone mass at unloaded condition and in the treatment of glucocorticoid as compared with those in wild-type mice.
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