Development of methods to prevent alveolar bone absorption during periodontitis using epigenetic regulation
| Project/Area Number |
21792160
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Social dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
TSUDA Hiromasa Nihon University, 歯学部, 助教 (60325470)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | ヒストンアセチル化 / ヒストンメチル化 / 細胞死 / 破骨細胞 / 予防法 / 骨破壞 / エピジェネティック / 分化 / 歯周炎 / 歯槽骨破壊 / 食品由来成分 / 破骨細胞分化 / 代謝調節因子 / 活性化剤・抑制剤 |
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| Research Abstract |
In this study, we examined a hypothesis that modulation of histone acetylation or methylation may also have some effect on the osteoclast differentiation. RANKL treatment induced the number of multinucleated osteoclast-like cells and the TRAP activities. Both histone deacetylase and methyltransferase inhibiton decreased the number of RANKL-induced osteoclast-like cells and TRAP activities in a dose-dependent manner. During the experiments, we also observed that RANKL treatment induced Raw264.7 cell death and the histone-deacetylase or histone methyltransferase-inhibitor dose-dependently suppressed the RANKL-induced cell death.
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Report
(3 results)
Research Products
(3 results)
