| Project/Area Number |
20390469
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
|
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| Research Institution | National Institute for Longevity Sciences,NCGG |
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Principal Investigator |
NIIDA Shumpei National Institute for Longevity Sciences,NCGG, 室長 (10137630)
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| Co-Investigator(Renkei-kenkyūsha) |
MIYAUCHI Mutsumi 広島大学, 大学院・医歯薬総合研究科, 准教授 (50169265)
SHIBAYAMA Keigo 国立感染症研究所, 部長 (50283437)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2010: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2009: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2008: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | 骨破壊 / 破骨細胞 / TLR / γ-GTP / バクテリア / 破骨細胞細胞 / 歯周炎 |
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| Research Abstract |
We found that bacterial gamma-glutamyl transpeptidase (bGGT) could induce osteoclast formation from the culture of bone marrow macrophages (BMMs). In the present study, we investigated the molecular mechanism of bGGT-mediated osteoclastogenesis. Because toll-like receptors (TLRs) are innate immune sensor for bacterial components, we firstly examined osteoclast induction test using BMMs derived from MyD88-deficient mice, which is a common adaptor molecule for several TLRs. The bGGT could not induce osteoclast formation in the cultures of these BMMs. To determine the bGGT specific receptor, we tested the osteoclast formation in TLR2- or TLR4-deficient BMMs. At last, we found that bGGT-dependent osteoclastogenesis did not occur in the TLR4- deficient BMMs. Furthermore, the phenotypes of signal transduction stimulated by bGGT were same as by LPS which is major ligand for TLR4. These results strongly suggest that bGGT stimulates osteoclastogenesis via TLR4.
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