Analyzes of periodontitis status from changes in gingival fibroblasts subpopulation

从牙龈成纤维细胞亚群变化分析牙周炎状态

• 批准号: 06671909
• 负责人: ARAI Hideo
• 金额: $ 1.41万
• 依托单位: Okayama University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671909/
• 关键词: Gingival fibroblast; subpopulation; IL-1beta; TNF-alpha; Prostaglandin E_2; レセプター; 亜群; PGE_2産生; コラーゲン合成

Tumor necrosis factor (TNF-alpha) has been known to stimulate prostaglandin production in gingival fibroblasts. In this study, we showed that, by the addition of interleukin-1beta (IL-1beta) into the culture, this enhancement was further augmented. IL-1beta decreased the number of TNF-alpha receptor and affinity to its ligand in gingival fibroblasts. We therefore examined the expression profile of IL-1 receptor mRNA and that of TNF-alpha receptor subtype mRNA under the absence or presence of IL-1beta to understand the underlying mechanisms by which IL-1beta modulate the responsiveness of gingival fibroblasts to TNF-alpha.Both type I and II TNF-alpha receptor mRNA were detected in gingival fibroblasts, but the expression of type I receptor was much more than that of type II.When gingival fibroblasts was stimulated by IL-1beta, the expression of type I TNF-alpha receptor was markedly depressed, while type II receptor was not affected.These results indicate that the initial observation that IL-1beta enhances the affinity of TNF-alpha to gingival fibrolasts (leading to increase of PGE_2 synthesis) can not be explained solely by the expression profile of TNF-alpha receptors.

已知肿瘤坏死因子（TNF-α）刺激牙龈成纤维细胞中的前列腺素产生。在这项研究中，我们发现，通过向培养物中加入白细胞介素-1 β（IL-1 β），这种增强作用进一步增强。IL-1 β降低牙龈成纤维细胞中TNF-α受体的数量及其与其配体的亲和力。因此，我们检测了IL-1 β存在或不存在时IL-1受体mRNA和TNF-α受体亚型mRNA的表达谱，以了解IL-1 β调节牙龈成纤维细胞对TNF-α反应性的潜在机制。IL-1 β刺激牙龈成纤维细胞后，I型TNF-α受体表达明显降低，这些结果表明，IL-1 β增强TNF-α对牙龈成纤维细胞的亲和力的初步观察结果，（导致PGE_2合成增加）不能仅用TNF-α受体的表达谱来解释。

项目成果

Takigawa,M.et al.: "Prostaglandin E_2 Inhibits Interleukin-6 Release But Not Its Transcription in Human Gingival Fibroblasts Stimulated With Interleukin-1β or Tumor Necrosis Factor-α" Journal of Periodontology. 65. 1122-1127 (1994)

Takikawa, M. 等人：“前列腺素 E_2 在用白细胞介素 1β 或肿瘤坏死因子 α 刺激的人牙龈成纤维细胞中抑制白细胞介素 6 的释放，但不抑制其转录”《牙周病学杂志》65。1122-1127 (1994)。

Takigawa, M., et al: "Prostaglandin E_2 inhibits interleukin-6 release but not its transcription in human gingival fibroblasts stimulated with interleukin-1beta or Lumor necrosis factor-alpha" J.Peridontol.65. 1122-1127 (1994)

Takikawa, M., 等人：“前列腺素 E_2 抑制白细胞介素 6 的释放，但不抑制其在用白细胞介素 1β 或肿瘤坏死因子 α 刺激的人牙龈成纤维细胞中的转录”J.Peridontol.65。

Takigawa,M et al.: "prostaglandin E_2 inhibits in terleukin-6 release but not its transcription in human gingival fibroblasts stimulated with Interleukin-1β or tumor necrosis facter-α." J. Periodontol.65. 1122-1127 (1994)

Takikawa, M 等人：“前列腺素 E_2 抑制白细胞介素 6 的释放，但不抑制白细胞介素 1β 或肿瘤坏死因子 α 刺激的人牙龈成纤维细胞的转录。J. periodontol.65 (1994)。

Takigawa,M. et al: "Cytokine-dependent synergistic regulation of interleukin-8 production from human gingival fibroblast.21GC02:J. Periodontol" 65. 1002-1007 (1994)

泷川，M.

Takigawa, M., et al: "Cytokine-dependent synergistie regulation of interleukin-8 production from human gingival fibroblasts." J.Peridontol.65. 1002-1007 (1994)

Takikawa, M. 等人：“人牙龈成纤维细胞产生白细胞介素 8 的细胞因子依赖性协同调节。”