The role of PRIP, a signaling molecule, in the regulation of osteoclast differentiation
| Project/Area Number |
17K11645
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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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| Research Field |
Functional basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
Matsuda Miho 九州大学, 歯学研究院, 准教授 (40291520)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 破骨細胞 / 分化 / Neuropirin 1 / PRIP / 骨代謝 / 共存培養 / 破骨細胞分化 / カルシウム / M-CSF / 細胞・組織 / 遺伝子 |
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| Outline of Final Research Achievements |
This study revealed the following: (i) an inositol 1,4,5-trisphosphate binding and signaling molecule, PRIP regulates nuclear translocation of NFATc1, a master regulator of osteoclast differentiation, through the change of intracellular Ca2+ concentration. (ii) PRIP is involved in the regulation of Semaphorin 3A-Neuropilin 1 signaling which regulates negatively osteoclast differentiation. The failure of these regulation by PRIP deficiency causes abnormal osteoclast differentiation to result in the impairment of osteoclastogenesis in KO mice.
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| Academic Significance and Societal Importance of the Research Achievements |
身体の支持組織でありかつ全身のエネルギー代謝を制御する組織でもある骨は、骨芽細胞と破骨細胞が担う骨形成と骨吸収のバランスで恒常性が維持されている。
シグナル分子PRIPの遺伝子欠損マウスにおいて骨量増加が認められたことから、PRIPの骨代謝制御への関わりについて研究を進め、今回の成果からPRIPが破骨細胞分化における特定の細胞内情報伝達経路の制御を担うことが明らかとなった。このことは、破骨細胞分化制御機構に新たな視点を見出し未知の分子基盤を導き出すものであり、破骨細胞が担う骨吸収機能の低下によって引き起こされる疾患の病因・病態の解明や治療の標的分子の発見など臨床応用にも貢献しうるものである。
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Report
(5 results)
Research Products
(31 results)
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[Journal Article] Osteocalcin triggers Fas/FasL-mediated necroptosis in adipocytes regulated by the activation of p300.2018
Author(s)
Otani, T., Matsuda, M., Mizokami, A., Kitagawa, N., Takeuchi, H., Jimi, E.,Inai, T., and Hirata, M.
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Journal Title
Cell Death Disease
Volume: 9
Issue: 12
Pages: 1194-1210
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] A peptide that blocks the interaction of NF-κB p65 subunit with Smad4 enhances BMP2-indeuce osteogenesis.2018
Author(s)
Urata M, Kokabu S, Matsubara T, Sugiyama G, Nakatomi C, Takeuchi H, Hirata TS, Aoki K, Tamura Y, Moriyama Y, Ayukawa Y, Matsuda M, Zhang M, Koyano K, Kitamura C, Jimi E.
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Journal Title
J Cell Physiol.
Volume: 1
Issue: 9
Pages: 1-11
DOI
Related Report
Peer Reviewed / Open Access
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