| Project/Area Number |
21390553
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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 |
Periodontal dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
IZUMI Yuichi 東京医科歯科大学, 大学院・医歯学総合研究科, 教授 (60159803)
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| Co-Investigator(Kenkyū-buntansha) |
NAGASAWA Toshiyuki 北海道医療大学, 准教授 (90262203)
KOBAYASHI Hiroaki 東京医科歯科大学, 医歯学総合研究科, 助教 (50396967)
IWASAKI Kengo 東京医科歯科大学, 医歯学総合研究科, 寄附講座教員 (40401351)
IWASAKI Kengo 東京医科歯科大学, 医歯学総合研究科, 助教 (50401378)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2011: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2009: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
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| Keywords | 歯周免疫機能学 / Wnt5a / 歯周炎 / 単球 / P. gingivalis LPS / P.gingivalis LPS / STAT1 / IFN-γ |
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| Research Abstract |
Wnt5a mRNA expression was up-regulated in chronic periodontitis tissue as compared to healthy control tissue. P. gingivalis LPS induced Wnt5a mRNA in the human monocytic cell line THP-1 with a peak at 4 hrs after stimulation. P. gingivalis LPS induced higher up-regulation of Wnt5a mRNA than E. coli LPS. The LPS receptors TLR2 and TLR4 were equally expressed on the surface of THP-1 cells. P. gingivalis LPS induced IkBa degradation and was able to increase the NF-kB binding activity to DNA. P. gingivalis LPS-induced Wnt5a expression was inhibited by NF-kB inhibitors, suggesting NF-kB involvement. Furthermore, IFN-g synergistically enhanced the P. gingivalis LPS-induced production of Wnt5a. Pharmacological investigation and siRNA experiments showed that STAT1 was important for P. gingivalis LPS-induced Wnt5a expression. These results suggest that the modulation of Wnt5a expression by P. gingivalis may play an important role in the periodontal inflammatory process and serve a target for the development of new therapies.
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