| Project/Area Number |
16591880
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Hokkaido University |
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Principal Investigator |
DEYAMA Yoshiaki Hokkaido Univ., Grad., Sch., Dent Med., Asso.Prof., 大学院・歯学研究科, 助教授 (80271667)
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| Co-Investigator(Kenkyū-buntansha) |
TOTSUKA Yasunori Hokkaido Univ., Grad., Sch., Dent Med., Prof., 大学院・歯学研究科, 教授 (00109456)
SUZUKI Kuniaki Hokkaido Univ., Grad., Sch., Dent Med., Prof., 大学院・歯学研究科, 教授 (40133748)
SHIBATA Kenichiro Hokkaido Univ., Grad., Sch., Dent Med., Prof., 大学院・歯学研究科, 教授 (50145265)
DOMON Takafumi Hokkaido Univ., Grad., Sch., Dent Med., Asso.Prof., 大学院・歯学研究科, 助教授 (50217618)
YOSHIMURA Yoshitaka Hokkaido Univ., Grad., Sch., Dent Med., Inst., 大学院・歯学研究科, 助手 (30230816)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Toll like receptor / Condensing osteitis / 骨芽細胞 / 線維芽細胞増殖因子2(FGF-2) / 石灰化 |
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| Research Abstract |
The aim of this project is to clarify the mechanisms of condensing osteitis crisis concerning to viral infection. Toll-like receptors (TLR) 1,3-7 expressed in osteoblastic MC3T3-E1 (E1) cells, TLR 1-7 in stromal ST2 cells, and TLR 3,6, and 7 in osteosarcoma cell, MG-63. TLR-3 expression is maximal in all of cells. When these cells were grown to confluent, and then treated with poly I:C for more two weeks, they formed mineralized nodules. It seems to be earlier than in control culture. DNA transfection experiments in with poly I:C treated-MG-63 cells were performed with reporter gene constructs containing 6 copies of cbfa1 or minimal alkaline phosphatase (ALP) promoter fragment. In both cases, the promoter activities increased. Moreover, it was shown using DNA microarray technology that poly I:C increased fibroblast growth factor 2 (FGF 2) mRNA expression in E1 cells. In addition, early growth response 1 (EGR 1), one of the transcription factors of FGF 2, protein expression also increased. Taken together, viral infection in bone tissue might cause to bone mineralization following to activate innate immunity systems of osteoblasts and stromal cells. It was suggested that activation of cbfa 1 following increase of FGF 2 production might be involved in this mechanism. More investigation with signal transduction systems in concerned with activation of FGF 2 signaling might need to elucidate these mechanism in detail.
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