2021 Fiscal Year Final Research Report
Elucidation of the molecular mechanism in the osteoclast function through protein kinase N3 and its clinical application.
| Project/Area Number |
19K10050
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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 57010:Oral biological science-related
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小林 泰浩 松本歯科大学, 総合歯科医学研究所, 教授 (20264252)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | 破骨細胞 / 骨吸収 |
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| Outline of Final Research Achievements |
In osteoporosis and inflammatory bone diseases, excessive bone resorption results in loss of bone mass. In order to prevent the deterioration of bone formation due to the failure of osteoclast-osteoblast coupling, it is necessary to develop a drug that suppresses only the bone-resorbing activity of osteoclasts. We found Protein kinase N3 (Pkn3), which enhances the function of osteoclasts downstream of the Wnt signaling. Since this protein is rarely expressed in normal tissues other than osteoclasts, it is suitable as a target for developing drugs with few side effects. In this research project, we administered a low-molecular-weight compound that had been reported to have a Pkn3 inhibitory effect on model mice showing bone loss due to increased bone resorption. This compound alleviated bone loss by suppressing bone resorption.
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| Free Research Field |
口腔生化学
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| Academic Significance and Societal Importance of the Research Achievements |
骨粗鬆症は、日本国内だけでも推定1000万人以上の患者さんが存在する疾患である。骨量の減少による、骨折の増加は、QOLを低下させるだけでなく、寝たきりにつながる可能性もある。骨量の減少は、骨吸収を行う破骨細胞の働きが、骨形成を行う骨芽細胞の働きを上回ることで生じるため、破骨細胞の骨吸収機能を抑制する化合物は、骨粗鬆症の治療薬になり得る。我々は、Pkn3というタンパク質が破骨細胞機能に重要であることを見出した。本研究はその阻害剤が、骨量減少モデルマウスの治療に利用できることを示したもので、臨床応用へつながる成果である。
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