2019 Fiscal Year Final Research Report
Elucidation of new bone mineralization mechanism using Podoplanin cKO mouse
Project/Area Number |
19K21419
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Project/Area Number (Other) |
18H06335 (2018)
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Multi-year Fund (2019) Single-year Grants (2018) |
Review Section |
0907:Oral science and related fields
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Research Institution | Fukuoka Dental College |
Principal Investigator |
Takara Kenyo 福岡歯科大学, 口腔歯学部, 助教 (30824164)
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Project Period (FY) |
2018-08-24 – 2020-03-31
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Keywords | ポドプラニン / CLEC-2 / 骨 |
Outline of Final Research Achievements |
We established the podplanin conditional knockout mouse Col1a11-Cre; PdpnΔ for the first time in the world. Calcification of Col1a11-Cre; PdpnΔ osteoblasts was suppressed by CLEC-2 in Pdpnfl mouse-derived osteoblasts, while Col1a11-Cre; PdpnΔ osteoblasts were not suppressed by CLEC-2. Calcium production and alkaline phosphatase activity of Pdpnfl-derived osteoblasts were suppressed by CLEC-2, but calcification and alkaline phosphatase activities of Col1a11-Cre; PdpnΔ-derived osteoblasts were not suppressed. We found that podoplanin was not concerned with hard tissue development although podoplanin was considered to be a functional molecule that regulates bone formation by CLEC-2.
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Free Research Field |
障害者歯科
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Academic Significance and Societal Importance of the Research Achievements |
ポドプラニンを骨において石灰化を制御する可能性のある新しい分子として位置づける事のできる成果を見出した可能性がある。これからの骨の研究に新しいツールを確立したと考える。ポドプラニンは血小板のCLEC-2と結合すると細胞の突起形成や骨格形成が弱まる事が知られており、本研究から、血小板が骨細胞に作用すると骨形成を抑制する可能性が考えられた。新しい骨の研究の道筋を作ったかもしれない。
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