| Project/Area Number |
24604002
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Mechanobiology
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| Research Institution | Nagasaki University |
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Principal Investigator |
MORIISHI Takeshi 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (20380983)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUDA Rika 活水女子大学, 健康生活学部・食生活健康学科, 教授 (30312838)
KOMORI Toshihisa 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (00252677)
MIYAZAKI Toshihiro 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (10174161)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 骨細胞ネットワーク / メカニカルストレス / 骨芽細胞 / 骨形成 / 骨吸収 / マイクロアレイ / 骨細胞 / 破骨細胞分化 |
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| Outline of Final Research Achievements |
We established human Bcl-2 transgenic mice under the control of mouse 2.3 kb Col1a1 promoter. Osteocyte processes were reduced depending on the expression levels of the transgene. We identified a novel mechanical stress-responsible genes, pyruvate dehydrogenase kinase 4 (Pdk4), FK506 binding protein 5 (Fkbp5), whose expression was upregulated in osteoblasts at the unloaded condition, using Bcl-2 transgenic mice with the disrupted osteocyte function. The bone of the Pdk4 KO mice normaly developed. At unloading, however, bone volume was reduced due to enhanced osteoclastogenesis and Rankl expression in wild-type mice but not in Pdk4 KO mice. These findings indicate that Pdk4 plays an important role in bone loss at unloading by promoting osteoclastogenesis. We analyze Fkbp5 KO mice now.
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