| Project/Area Number |
23592240
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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 |
Orthopaedic surgery
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| Research Institution | Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology |
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Principal Investigator |
YORITO Anamizu 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 (70302693)
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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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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | シグナル伝達 / 破骨細胞 |
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| Research Abstract |
AMPK is a metabolic master switch that mediates the adaptation of the cell to variations in the nutritional environment. Its activity is stimulated by increases in the intracellular AMP/ATP ratio in response to stresses such as exercise, hypoxia, and glucose deprivation. To test whether modulating AMPK activity would affect osteoclast function, we used adenovirus vectors containing dominant negative (a1DN , a2DN) or constitutively active (a1CA , a2CA) forms of AMPK catalytic subunits (a1 and a2). The phosphorylation level of acetyl-CoA carboxylase at Ser-79, a direct target of AMPK, was modulated by adenovirus-mediated expression of the AMPK mutants. Modulation of AMPK activity did not affect osteoclast survival or bone resorption, indicating that AMPK is not involved in ATP depletion-induced bone resorption.
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