2021 Fiscal Year Final Research Report
Regulation of bone formation and osteocyte function by nuclear protein involved in sclerostin regulation
| Project/Area Number |
19K09553
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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 56020:Orthopedics-related
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
久木田 明子 佐賀大学, 医学部, 寄附講座教授 (30153266)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | 骨代謝 / 骨細胞 / 転写制御因子 / 骨粗鬆症 |
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| Outline of Final Research Achievements |
We analyzed the role of transcriptional regulator Nupr1 in osteocytes and osteoblasts. Nupr1 was highly expressed in osteocytes and osteoblasts expressing screrostin. Nupr1 overexpression promoted screrostin expression, and the expression of Wnt signaling molecules was reduced in osteoblasts derived from Nupr1 knockout mice. In addition, expression of cytoskeleton proteins, its regulatory proteins, and proteases which are thought to be involved in bone formation, was decreased in osteocytes derived from Nupr1 knockout mice. The results suggest that Nupr1 is involved in bone formation by regulating the function of osteocytes through the control of cytoskeleton organization and protease production.
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| Free Research Field |
整形外科学
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| Academic Significance and Societal Importance of the Research Achievements |
超高齢化社会に伴い、骨粗鬆症などの骨・関節疾患の患者数が増加し、重大な社会問題となっている。近年、骨吸収を行う破骨細胞と骨形成を行う骨芽細胞に加えて、骨の中に最も多く存在し、神経細胞のようなネットワークを形成する骨細胞が骨代謝や骨のホメオスタシスに重要な役割を持つことが考えられている。本研究では、マウスで遺伝子を欠損すると骨形成が亢進するNupr1という転写制御因子の骨芽細胞と骨細胞での発現とNupr1による骨形成の新たな制御機構を明らかにした。本研究の結果は、骨粗鬆症や変形性関節症などの骨・関節疾患の病態の解明や新たな治療法の開発などに将来的に寄与するものと考えられる。
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