| Project/Area Number |
22592071
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOMORI Toshihisa 長崎大学, 医歯薬学総合研究科, 教授 (00252677)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | カルシウムチャンネル / 破骨細胞 / カルシウムシグナル / カルシウム / 骨代謝 / TRPV4 |
|---|
| Research Abstract |
Osteoclast differentiation is critically dependent on calcium (Ca2+) signaling. Transient receptor potential vaniroid (TRPV) 4, mediates Ca2+ influx in the late stage of osteoclast differentiation, thereby regulates Ca2+ signaling. However, the system-modifying effect of TRPV4 activity remains to be determined. Bone loss due to TRPV4 activation was abrogated by loss of interactions between Ca2+/calmodulin signaling and TRPV4. Finally, modulators of TRPV4 interactions with the calmodulin-binding domain were investigated by proteomic analysis. Non-muscle myosin IIa was then identified by LC-MS/MS analysis, which was confirmed by immunoblotting following coimmunoprecipitation with TRPV4. These results indicate that TRPV4 activation reciprocally regulates Ca2+/calmodulin signaling, which involves an association of TRPV4 with myosin IIa, and promotes sufficient osteoclast function.
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