Project/Area Number |
17K19695
|
Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
|
Allocation Type | Multi-year Fund |
Research Field |
Surgery of the organs maintaining homeostasis and related fields
|
Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
Hayashi Mikihito 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (50581914)
|
Project Period (FY) |
2017-06-30 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
|
Keywords | 破骨細胞 / 骨生物学 |
Outline of Final Research Achievements |
Although much knowledge has been obtained from animal models, therapeutic targets studied in mice often fail to confirm their effects in humans. Therefore, it is possible that we have overlooked an important part of human-specific genes. In this study, we performed gene expression analysis of human bone cells to examine specific functional genes and identified the human-specific factor X. X is a soluble factor, and its target molecule Y has the ability to promote osteoclast differentiation both in human and mouse cells. We found that X significantly suppresses osteoclast differentiation by specifically suppressing the function of Y. Thus, X may be a factor characterizing human osteoclast differentiation.
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Academic Significance and Societal Importance of the Research Achievements |
近年、骨代謝学領域に限らず、マウスで同定・開発された治療標的の多くがヒトの疾患において効果が確認されない事実が問題視されている。骨生物学領域のほとんどの研究でもマウス細胞が用いられており、骨構成細胞のヒトとマウスの明らかな違いから、重要なヒト遺伝子を見落としている可能性が示唆されていた。 本研究で構築したヒト骨構成細胞遺伝子発現プロファイリングにより、ヒト特異的機能未知遺伝子が解明され、ヒト骨構成細胞特異的な分子メカニズムの解明につながる可能性がある。さらに、より確実な治療戦略への道筋となることが期待される。
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