| Project/Area Number |
23593039
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
MAKI kenshi 九州歯科大学, 歯学部, 教授 (60209400)
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| Co-Investigator(Kenkyū-buntansha) |
EIJIRO Jimi 九州歯科大学, 歯学部, 教授 (40276598)
HIDEFUMI Fukushima 九州歯科大学, 歯学部, 助教 (70412624)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 破骨細胞 / c－Src / p130Cas / アクチン / 大理石骨病 / ステロイド / 顎骨 / c-Src / Pyk2 / インテグリン / osteoclast / Bone resorption / Actin cytoskeleton |
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| Research Abstract |
To investigate the role of p130Cas on osteoclastic bone resorption, we generated osteoclast-specific p130Cas conditional knockout (p130CasOCL-) mice. p130CasOCL- mice exhibit a high bone mass phenotype caused by defect in multinucleation and cytoskeleton organization causing bone resorption deficiency. Bone marrow cells from p130CasOCL- mice were able to differentiate into osteoclasts in vitro. However, osteoclasts from p130CasOCL- mice failed to form actin rings and resorb pits on dentine slices. Although the initial events of osteoclast attachment, such as ntegrin or Src phosphorylation, were intact, the Rac1 activity that organizes the actin cytoskeleton was reduced, and its distribution was disrupted in p130CasOCL- osteoclasts. Dock5, a Rho family guanine nucleotide exchanger, failed to associate with Src or Pyk2 in osteoclasts in the absence of p130Cas. These results strongly indicate that p130Cas plays pivotal roles in osteoclastic bone resorption.
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