| Project/Area Number |
24659829
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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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, 教授 (00252677)
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| Co-Investigator(Kenkyū-buntansha) |
MORIISHI Takeshi 長崎大学, 大学院医歯薬学総合研究科, 助教 (20380983)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 骨細胞 / 破骨細胞 / 廃用性骨粗鬆症 / メカニカルストレス / Pdk4 |
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| Research Abstract |
Bone mass is increase by exercise and reduced by long-term bed rest, immobilization caused by nerve injury, and microgravity in the space. These non-weight bearing conditions cause disuse osteoporosis. Osteocyte network, which is embedded in bone, is responsible for the sensing of mechanical stress and the transduction of the signal to osteoblasts and osteoclasts in the bone surface, and regulates bone mass. Pdk4, which is a kinase that inhibits energy production in mitochondria, was upregulated in osteoblasts and osteocytes in the unloaded condition of adult mice. Bone loss in the unloaded condition was not caused in Pdk4 adult knockout mice, indicating that Pdk4 is involved in bone loss in the unloaded condition of adult mice.
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