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2004 Fiscal Year Final Research Report Summary

Molecular biological analysis of dentin hypersensitivity

Research Project

Project/Area Number 14370620
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Conservative dentistry
Research InstitutionKagoshima University

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)

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)
Project Period (FY) 2002 – 2004
KeywordsDentin Hypersensitivity / DNA microarray / IP6K-1 / Mechanism
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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Published: 2006-07-11  

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