Molecular biological analysis of dentin hypersensitivity

2004 Fiscal Year Final Research Report Summary

• Project/Area Number: 14370620
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Conservative dentistry
• Research Institution: Kagoshima 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
• Keywords: Dentin 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.