Regulation of bone and cartilage formation by ADAM10
| Project/Area Number |
26462318
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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 |
Orthopaedic surgery
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| Research Institution | Keio University |
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Principal Investigator |
Yoda Masaki 慶應義塾大学, 医学部(信濃町), 助教 (30464994)
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| Co-Investigator(Kenkyū-buntansha) |
堀内 圭輔 慶應義塾大学, 医学部(信濃町), 特任准教授 (30327564)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ADAM10 / 骨・軟骨代謝 / シェディング / Notchシグナル / 破骨細胞分化 / 細胞分化 / Notch / シグナル伝達 / 発生・分化 |
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| Outline of Final Research Achievements |
In this study, we analyzed the regulation mechanisms of bone / cartilage formation and osteoclast differentiation by membrane type metalloprotease ADAM10. Analysis of mice abrogated ADAM10 in cartilage revealed that ADAM10 is essential for final differentiation of chondrocytes. In addition, analysis of osteoblast-specific ADAM10 deficient mice revealed that these mice indicated an increase in TSLP concentration in the serum and exhibited severe dermatitis. Furthermore, the experiment for osteoclast differentiation using osteoclast precursor lacking ADAM10 revealed that the signaling from Notch receptor, which is one of substrates for ADAM10, on the cell membrane of osteoclast precursor completely suppresses osteoclast differentiation.
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Report
(4 results)
Research Products
(2 results)
