Molecular biological analysis of dentin hypersensitivity

牙本质过敏的分子生物学分析

• 批准号: 14370620
• 负责人: TORII Mitsuo
• 金额: $ 8.64万
• 依托单位: Kagoshima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2004
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14370620/
• 关键词: Dentin Hypersensitivity; DNA microarray; IP6K-1; Mechanism

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.

我们在牙龈成纤维细胞中发现了一个新的基因，该基因与中央神经突触的可塑性和外周神经上的痛觉过敏密切相关。该分子与肌醇六磷酸磷酸酶-1（IP6K-1）具有很高的同源性，与钙离子通道的激活有关。因此，该分子有可能增加对外部刺激的敏感性，并在感觉神经上引起痛觉过敏。我们还透露，在培养的幼犬细胞和牙龈成纤维细胞中，IP6K-1在炎症的急性期强烈表达。 HELA细胞被证实，IP6K-1通过诱导IP6K-1质粒而表达过度。通过过氧化氢抑制了IP6K-1在表达的HELA细胞上的凋亡，并通过脂多糖和肿瘤坏死因子-A胞外IL-8的胞吐作用增加了。这些结果表明，IP6K-1与细胞的存活以及纸浆和牙龈细胞的炎症有关。