Regulation of bone resorption by membrane reparing molecules: Live imaging of the specific fusion among osteoclast precursors
| Project/Area Number |
24659816
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
KUKITA TOSHIO 九州大学, 歯学研究科(研究院), 教授 (70150464)
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| Co-Investigator(Kenkyū-buntansha) |
KUKITA Akiko (30153266)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 破骨細胞 / 分化 / 膜融合 / 膜修復 / MG53 / 骨吸収制御 / 膜修復分子 / 細胞融合 / 膜ナノチューブ / M53 / DC-STAMP / アポトーシス / 細胞分化 |
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| Research Abstract |
When the muscle cell membrane was subjected to the damage, the membrane was immediately repaired by the action of "membrane repairing molecules". Osteoclasts are formed by fusion of mononuclear osteoclast precursors, and this process is postulated to be guarranteed by the action of "membrane reparing mechanisms". The purpose of this research is to identify MG53 or its analogue and involvement of membrane repairing mechanism" during the process of osteoclast differentiation. Unstimulated osteoclast precursors expressed MG53. However, its expression was dramatically suppressed after being stimulated to form osteoclasts. Our data suggested that the "membrane repairing molecule" could act as the negative regulator for osteoclast differentiation.
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Report
(3 results)
Research Products
(27 results)
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[Journal Article] Mesenchymal stem cells markedly suppress inflammatory bone destruction in rats with adjuvant-induced arthritis.2014
Author(s)
Takano, T. Li, Y. J. Kukita, A. Yamaza, T. Ayukawa, Y. Moriyama, K. Uehara, N. Nomiyama, H. Koyano, K. and Kukita, T.
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Journal Title
Lab. Invest.
Volume: 94
Pages: 286-296
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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