| Project/Area Number |
22659268
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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 |
Orthopaedic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Sakae 東京大学, 医学部附属病院, 教授 (50282661)
HIROTA Jinsou 東京大学, 医学部附属病院, 医員 (30570733)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,160,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | 破骨細胞 / Bcl-2 family蛋白 / Bim / Puma / Bcl-2 family |
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| Research Abstract |
The Bcl-2 family proteins are known as key regulators of apoptosis. In osteoclasts, Bcl-2 family proteins were reported to regulate not only cell viability but also bone resorbing activity. To determine the role of pro-apoptotic Bcl-2 family proteins Bim and Puma, we made knock-out mouse and evaluate bone morphometry, osteoclast viability and bone resorbing activity. Bim KO mice showed mild osteosclerosis due to impaired bone resorption, despite their osteoclast survival were extended. Puma KO mouse had no phenotype in bone morphometry. Puma KO osteoclast had extended viability but there were no significant difference in bone resorbing activity.
Making Bim and Puma double knock-out mouse(Bim-/-Puma-/-) are required for further understanding of the co-regulation between Bim and Puma in osteoclast.
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