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Identification of switching factor that determinates life and death of human dental pulp cells

Identification of switching factor that determinates life and death of human dental pulp cells
确定人牙髓细胞生死的转换因子
批准号:
17591998
负责人:
TOKUBA Masayuki
金额:
$2.24万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2005
资助国家:
日本
项目状态:
已结题
起止时间:
2005 至 2006

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中文摘要
翻译
阿南达胺(AEA)可触发细胞凋亡。本研究旨在探讨其受体在乙酸乙酯诱导人牙髓细胞(HPC)凋亡中的作用及其信号转导途径。AEA可明显诱导HPC凋亡。CB2拮抗剂和VR1拮抗剂均可抑制AEA诱导的细胞死亡。一种细胞外信号调节激酶(ERKs)的抑制剂显著地阻止了HPC细胞的死亡。ERK抑制剂和CB2拮抗剂可抑制AEA调节的核因子-kappaB(NF-κB)激活。此外,针对NF-κB亚单位的特异性siRNA(p50和p65)可抑制AEA诱导的HPC细胞死亡。在这一点上,AEA诱导的牙髓细胞凋亡是通过NF-κB依赖和非依赖的途径来调节的,底物P(SP)诱导与牙髓炎症有关的促炎细胞因子的表达,如白介素6(IL-6)。为了确定SP诱导IL-6的信号通路,我们检测了人牙髓细胞(PF-10)中丝裂原活化蛋白激酶(MAPKs)的活性。SP可在5min内诱导p38MAPK的磷酸化,这种激活可持续至40min,且不依赖于SP刺激PF-10细胞后诱导的细胞外信号相关蛋白(ERK-1和ERK-2)的激活。凝胶迁移率改变分析显示,p38MAPK不参与SP诱导的核因子-kappaB(NF-κB)的激活。然而,p38MAPK介导了SP诱导的IL-6的产生,这一点可以通过使用该激酶的特异性抑制剂来证明。我们的结果提示,p38MAPK的激活对于非NF-κB调节牙髓组织神经源性炎症具有重要意义。
英文摘要
Anandamide (AEA) triggers apoptosis. Here, we aim to investigate the role of its receptors on ANE-induced apoptosis and its signaling pathway in human dental pulp cells (HPC). AEA clearly induced apoptosis on HPC. Both CB2 antagonist and VR1 antagonist inhibited AEA-induced cell death. An inhibitor of extracellular signal-regulated kinases (ERKs) significantly prevented HPC cell death. ERK inhibitors and CB2 antagonist inhibited AEA-regulated nuclear factor-kappa B (NF-κB) activation. Furthermore, specific siRNA for NF-κB suunits (p50 and p65) inhibited AEA-induced HPC cell death. In this regard, AEA-induced pulp apoptosis was regulated by NF-κB-dependent and-independent pathways.Substance P (SP) induces the expression of proinflammatory cytokines, such as interleukin (IL)-6, which are implicated in pulp inflammation. To determine the signal pathway of SP-induced IL-6, we examined the activities of the mitogen-activated protein kinases (MAPKs) in human dental pulp cell (PF-10) cultures. SP induced the phosphorylation of p38 MAPK within 5 min; this activation persisted for up to 40 min and was independent of the activation of extracellular signal-related kinases (ERK-1 and ERK-2), which was induced after SP stimulation of PF-10 cells. As shown by electrophoresic mobility shift assay (EMSA), p38 MAPK was not involved in SP-induced activation of nuclear factor-kappa B (NF-κB). However, p38 MAPK mediated SP-induced IL-6 production, as shown by the use of specific inhibitors of this kinase. Our results suggest that the activation of p38 MAPK is important for NF-κB-independent regulator of neurogenic inflammation in dental pulp tissues.
期刊论文(3)
专著(0)
科研奖励(0)
会议论文
培養歯髄細胞におけるサブスタンスPのIL-6誘導に対するMAPキナーゼと転写因子の関与
MAP 激酶和转录因子参与培养牙髓细胞中 P 物质诱导 IL-6 的过程
DOI: --
发表时间: 2006
期刊: 日本歯科保存学会誌 49・4
影响因子: --
作者: [徳田雅行, 作田哲也, 小山徹, 達山祥子, 長岡成孝, 鳥居光男]
通讯作者: 鳥居光男
DOI: 10.1080/03008200500182490
发表时间: 2005-01
期刊: Connective Tissue Research
影响因子: 2.9
作者: [M. Tokuda;R. Miyamoto;T. Sakuta;S. Nagaoka;M. Torii]
通讯作者: M. Tokuda;R. Miyamoto;T. Sakuta;S. Nagaoka;M. Torii
国内基金
海外基金
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