2023 Fiscal Year Final Research Report
The study of the normal regulatory mechanism in the alveolar bone by PDPN-dependent mechanosensing
| Project/Area Number |
21K10153
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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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| Review Section |
Basic Section 57070:Developmental dentistry-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
佐藤 嘉晃 北海道大学, 歯学研究院, 教授 (00250465)
沢 禎彦 岡山大学, 医歯薬学域, 教授 (70271666)
足利 雄一 北海道大学, 大学病院, 講師 (70372258)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | ポドプラニン / 骨細胞突起 / ポドプラニン欠損マウス |
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| Outline of Final Research Achievements |
In this study, it was found that the extension of cell process elongation of osteoblasts was inhibited by CLEC-2. This led to the consideration that podoplanin might affect osteoblast process formation. Dmp1-Cre;PdpnΔ/Δ mice ( podoplanin - conditional knockout mice ) used in this study showed no differences in body growth, and there were no differences in calcification or alkaline phosphatase activity of osteoblasts. However, the extension of osteoblast processes was suppressed. Electron microscopy observation revealed no differences in bone matrix formation or distribution of osteocytes, but in Dmp1-Cre;PdpnΔ/Δ mice, the number and thickness of osteocyte processes were fewer and finer compared to wild-type mice, suggesting that podoplanin may be involved in the formation of osteocyte networks.
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| Free Research Field |
歯科矯正学
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| Academic Significance and Societal Importance of the Research Achievements |
ポドプラニンは骨細胞マーカーとして知られるものの、石灰化への関与は未開拓である。本研究は、Dmp1-Cre;PdpnΔ/Δマウス（ポドプラニン欠損マウス）を応用し、ポドプラニンを新機軸に石灰化制御のメカノトランスダクション経路を開拓するところに学術的意義がある。また、矯正学的メカニカルストレス環境にある顎骨のリモデリングにおいて、１）骨細胞マーカーポドプラニンがメカニカルストレスを石灰化信号に変換、２）造血系細胞と破骨細胞が発現するポドプラニン受容体CLEC-2がこれをキャンセルする、と考えたことに創造性、社会的意義があると考える。
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