Substance P Activates p38 Mitogen-Activated Protein Kinase to Promote IL-6 Induction in Human Dental Pulp Fibroblasts
Substance P Activates p38 Mitogen-Activated Protein Kinase to Promote IL-6 Induction in Human Dental Pulp Fibroblasts
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DOI：
10.1080/03008200500182490
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发表时间：
2005-01
影响因子：
2.9
通讯作者：
M. Tokuda;R. Miyamoto;T. Sakuta;S. Nagaoka;M. Torii
中科院分区：
文献类型：
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作者：
M. Tokuda;R. Miyamoto;T. Sakuta;S. Nagaoka;M. Torii
P物质（SP）诱导促炎细胞因子的表达，如白细胞介素（IL）-6，这与牙髓炎症有关。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）培养物中丝裂原活化蛋白激酶（MAPK）的活性。SP在5分钟内诱导p38 MAPK磷酸化，这种激活持续长达40分钟，并且不依赖于SP刺激PF-10细胞后诱导的细胞外信号相关激酶（ERK-1和ERK-2）的激活。电泳迁移率变动分析显示p38 MAPK不参与SP诱导的核因子-κ B（NF-κB）活化。然而，p38 MAPK介导SP诱导的IL-6产生，如通过使用该激酶的特异性抑制剂所示。我们的研究结果表明，p38 MAPK的激活是重要的NF-κ B的非依赖性调节神经源性炎症牙髓组织。
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) that were induced after SP stimulation of PF-10 cells. As shown by electrophoretic mobility shift assay 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.