The infection defense mechanism by salivary gland secretion antibacterial proteins in the junctional epithelium

唾液腺分泌交界上皮抗菌蛋白的感染防御机制

• 批准号: 24890244
• 负责人: NISHII Kousuke
• 金额: $ 1.91万
• 依托单位: Showa University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-08-31 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24890244/
• 关键词: 歯周病; 付着上皮; レーザーマイクロダイセクション; プロラクチン誘導タンパク; マイクロアレイ; 抗菌タンパク

A quantitative analysis of Proractin induced protein(PIP) mRNA in junctional epithelium (JE) and oral gingival epithelium (OGE) of both conventional mice and germ-free mice was performed using laser microdissection and real-time polymerase chain reaction. Real-time PCR analysis indicated that PIP expressions were mainly detected in JE ofconventional mice not detected in OGE. Expression of PIP after LPS stimulation in cuitured human oral epithelial cells was higher expression most 24 hours after stimulation.Further, the results of immunohistochemical analysis, expression of PIP was observed in JE of each of the conventional mice and germ-free mice, expression was not observed in the OGE,respectively.

采用激光显微切割和实时荧光定量聚合酶链反应技术对正常小鼠和无菌小鼠口腔粘膜结合上皮（JE）和牙龈上皮（OGE）中的普拉卡汀诱导蛋白（PIP）mRNA进行定量分析。实时荧光定量PCR分析表明PIP主要在普通小鼠的乙脑中表达，而在OGE中未检测到。LPS刺激后培养的人口腔上皮细胞PIP表达最高，最多在刺激后24 h表达，免疫组化分析结果显示，PIP在常规小鼠和无菌小鼠的JE中均有表达，而在OGE中无表达。

项目成果

TNF-α induces RANKL Expression in Gingival Epithelial Cells through PKA Signaling

TNF-α 通过 PKA 信号传导诱导牙龈上皮细胞 RANKL 表达

• 发表时间: 2012
• 作者: 藤原亮一; 臼井通彦; 西井浩介; 塚本康巳;山本松男
• 通讯作者: 山本松男

再構成歯胚の萠出により形成された接合上皮は歯原性上皮由来である

重建牙胚萌出形成的连接上皮来源于牙源性上皮

• 发表时间: 2013
• 期刊: Dental Medicine Research
• 作者: 八島 沙羅;山本 剛;西井 浩介;古屋 まど香;田中 準一;山本 松男;立川 哲彦;美島 健二
• 通讯作者: 美島 健二