| Project/Area Number |
18592047
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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 | Showa University |
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Principal Investigator |
TAKAMI Masainichi Showa University, School of Dentistry, Lecturer (80307058)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIJO Ryutaro Showa University, School ofDentistry, Professor (70233939)
YAMADA Atsushi Showa University, School of Dentistry, Lecturer (50407558)
SUZAWA Tetsuo Showa University, School of Dentistry, Lecturer (60271285)
MIYAMOTO Yoichi Showa University, School of Dentistry, Associate Professor (20295132)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Bone metabolism / Innate immunity / Osteoclasts / Transcription factor / Gene expression / Cellular differentiation / Dendritic cells / Teeth / 免疫 / 骨破壊 / 遺伝子 / 炎症 |
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| Research Abstract |
Severe bone destruction is often induced by enhanced osteoclast formation under the inflammatory conditions. Therefore, elucidation of the mechanism of osteoclastogenesis will contribute to the development of methods for the treatment of diseases that accompanies bone destruction. Monocytes and macrophages are known to differentiate into not only osteoclasts but also dendritic cells that play roles of immune responses. We analyzed the changes of cellular characteristics during osteoclastogenesis and dendritic cell differentiation from common precursors. It was found that the potential of dendritic cell differentiation was lost within 24h after beginning of osteoclastogenesis. The characteristics of these cells are quite unique because the cells possessed phagocytic function as well as macrophages but they required RANKL stimulation to survive like osteoclasts. Furthermore, we analyzed mRNA expressions during osteoclastogenesis and dendritic cell differentiation using DNA microarray technique. A transcription factor, IRF-8 was found to be downregulated during osteoclastogenesis but not in dendritic cell differentiation. The IRF-8 deficient mice exerted severe osteoporosis due to enhanced osteoclastogenesis. Moreover, over-expression of IRF-8 in osteoclast precursors strongly suppressed osteoclastogenesis but not dendritic cell differentiation. These results suggest that IRF-8 plays roles of suppression of osteoclastogenesis but not dendritic cell differentiation. These findings will contribute to establishment of new methods for the treatment of periodontal diseases and rheumatoid arthritis.
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