| Project/Area Number |
16K20609
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
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| Research Collaborator |
Ohba Shinsuke
Yamakawa Akira
Tei Yuichi (Chung Ung-il)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | カップリングファクター / Ihh / 破骨細胞 / コンディショナルノックアウトマウス / 破骨細胞特異的ノックアウトマウス / Ihhノックアウトマウス / 歯学 / 骨代謝 / 破骨細胞－骨芽細胞カップリングファクター |
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| Outline of Final Research Achievements |
Bone remodeling is a part of bone metabolism and osteoblast to osteoclast signal transduction has been study intensively. Various kinds of factors had been suggested as coupling factor for this phenomenon. However osteoclast to osteoblast type of signal transduction has yet to be elucidate. We discovered that Indian hedgehog, a protein that has an important role in osteoblast differentiation, is upregulated during osteoclast differentiation. And the secrete protein can lead osteoblast differentiation in vitro. We generated a conditional knockout mouse by crossing RANK-Cre and Ihh-flox mouse in order to confirm whether osteoclastic Ihh would influence bone formation in vivo. In P0 littermates, less bone formation has been observed comparing to control mouse. These results suggests that Ihh is a candidate of osteoclast to osteoblast type of coupling factore. We are now under investigating the osteoclastic Ihh effect on adult mice.
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| Academic Significance and Societal Importance of the Research Achievements |
骨組織維持機構の一端として骨リモデリング現象が起こることが知られており、骨芽細胞から破骨細胞へのシグナル伝達メカニズムについては解析が盛んに進められてきた。カップリングファクターとして様々な分子の存在が示唆されているが、破骨細胞から骨芽細胞へのシグナル伝達の方法は明らかにされていなかった。今回の発見では破骨細胞から始まる一連の骨リモデリングが開始されるメカニズムの一端を見出したに過ぎないが、より効率的な骨再生療法や骨粗鬆症の病態理解、および治療法開発に重要な知見となると考えている。
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