| Project/Area Number |
16K20067
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Saitama Medical University |
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Principal Investigator |
Kuratani Mai 埼玉医科大学, 医学部, ポストドクター (50758109)
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| Research Collaborator |
KATAGIRI Takenobu 埼玉医科大学, 医学部, 教授
TSUKAMOTO Sho 埼玉医科大学, 医学部, 助教
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨格筋 / 異所性骨化 / BMP / 進行性骨化性線維異形成症 / 軟骨・骨 / 炎症 / 骨・軟骨代謝 |
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| Outline of Final Research Achievements |
Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder characterized by progressive heterotopic ossification (HO) in soft tissues, such as skeletal muscle, especially after trauma. A gain-of-function mutation in ALK2, ALK2(R206H), is commonly found in patients with typical FOP. ALK2 is a type I receptor of BMP and transduces osteogenic signaling. In the present study, we observed that expression levels of BMP-2 and BMP-7 increased in injured muscle. In vivo implantation of BMP-2 and BMP-7-containing pellets drove HO in skeletal muscle. We analyzed their biological activity on ALK2(R206H) in vitro, BMP-7, induced BMP-specific luciferase reporter activities in C2C12 cells expressing human ALK2(R206H). In conclusion, BMP-7, which increased in injured muscle, contribute to the muscle trauma-induced HO in FOP.
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