| Project/Area Number |
14370620
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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 |
Conservative dentistry
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| Research Institution | Kagoshima University |
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Principal Investigator |
TORII Mitsuo Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (30116066)
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| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Ikuro Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (20082282)
IMAMURA Takatoshi Kumamoto University, Faculty of Medical and Pharmaceutical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (20176499)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2004: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2002: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | Dentin Hypersensitivity / DNA microarray / IP6K-1 / Mechanism |
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| Research Abstract |
We found a novel gene in gingival fibroblast, which was deeply concerned with plasticity of central nerve synapses and hyperalgesia on peripheral nerves.
This molecule has high homology with inositol hexakisphosphatase-1 (IP6K-1), which is concerning with activation of calcium ion channel. Therefore there is a possibility for this molecule to increase the sensitivity to external stimuli and cause hyperalgesia on sensory nerves. We also revealed that IP6K-1 is strongly expressed at acute phase of inflammation in cultured pup cell and gingival fibroblast. Hela cells were confirmed that IP6K-1 was over expressed by induction of IP6K-1 plasmid. Apoptosis of IP6K-1 over expressed Hela cell by hydrogen peroxide was inhibited and exocytosis of IL-8 by lipopolysaccharide and tumor necrosis factor-a was increased. Theses results suggested that IP6K-1 is concerned with survival of cells and inflammation of pulp and gingival cells.
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