| Project/Area Number |
15K07950
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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 |
Biological pharmacy
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| Research Institution | Hoshi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
内田 隆史 東北大学, 農学研究科, 教授 (80312239)
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| Co-Investigator(Renkei-kenkyūsha) |
Amano Hitoshi 大阪歯科大学, 歯学部, 准教授 (90212571)
Takahashi Noriko 星薬科大学, 薬学部, 教授 (50277696)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 骨代謝 / p57Kip2 / Pin1 / 細胞周期 / 骨粗鬆症 / 骨芽細胞 / 破骨細胞 |
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| Outline of Final Research Achievements |
We expected that suppression of p57Kip2 could increase osteoblastic proliferation, resulted in improvement of osteoporosis patients. A cell cycle regulator, p57Kip2-null mice had osteoblasts with high proliferation rates and their osteoclasts maturation were less than the wild-type mice. On the other hand, a cell cycle acceleration prolyl isomerase, Pin1-null mice displayed typical osteoporotic symptoms with many maturated osteoclasts. Then we created p57Kip2/Pin1 double deficient mice, which also showed the phenotypes similar to p57Kip2-null mice. So we thought that p57Kip2 might be under Pin1 in osteoblasts,and the osteoporosis with Pin1 inactivation could be improved by p57Kip2 suppression.
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