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首页> 外文期刊>Journal of Cellular Physiology >Interleukin-17A stimulates migration of periodontal ligament fibroblasts via p38 MAPK/NF-κB -dependent MMP-1 expression
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Interleukin-17A stimulates migration of periodontal ligament fibroblasts via p38 MAPK/NF-κB -dependent MMP-1 expression

机译：Interleukin-17A刺激迁移通过p38牙周韧带成纤维细胞MAPK / NF -κB端依赖金属蛋白酶- 1的表达

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摘要

Interleukin-17 (IL-17) is a cytokine secreted predominantly by Th17 cells. Although IL-17 is primarily associated with the induction of tissue inflammation, the other biological functions of IL-17, including its wound-healing functions, have yet to be thoroughly explored. Fibroblast proliferation and migration play essential roles in periodontal wound-healing responses. In this study, we report that IL-17A can increase the migration and expression of matrix metalloproteinase (MMP)-1 in human periodontal ligament (PDL) fibroblasts but has no effect on PDL fibroblast proliferation. IL-17A-induced MMP-1 expression led to cell migration, which was attenuated by pre-treatment with IL-17 receptor neutralizing antibody and small interfering RNA (siRNA) for MMP-1. The IL-17A-induced cell migration was also attenuated by its tissue inhibitor of matrix metalloproteinase (TIMP)-1. In addition, a p38 mitogen-activated protein kinase (MAPK) inhibitor (SB203580) inhibited IL-17A-induced increase of the migration and MMP-1 upregulation of PDL fibroblasts. The involvement of p38 MAPK in IL-17A-induced MMP-1 expression and cell migration was further confirmed by transfection of p38α siRNA. A nuclear factor kappaB (NF-κB) inhibitor (pyrrolidine dithiocarbamate) also suppressed the cell migration and MMP-1 expression enhanced by IL-17A. Moreover, transfection with p38α siRNA inhibited IL-17A-induced NF-κB nuclear translocation as well as NF-κB binding activity. Our results suggest that IL-17A enhances the migration of PDL fibroblasts by increasing MMP-1 expression through the IL-17 receptor, p38 MAPK, and NF-κB signal transduction pathways.
机译：Interleukin-17 (IL-17)是一种细胞因子分泌主要由Th17细胞。主要与感应相关的组织炎症,其他的生物功能IL-17,包括其愈合的功能,尚未进行过彻底的探索。扩散和迁移发挥重要作用在牙周愈合反应。研究中,我们报告,IL-17A可以增加迁移和矩阵的表达式在人类牙周金属蛋白酶(MMP) 1韧带(PDL)成纤维细胞但没有影响PDL纤维母细胞增殖。金属蛋白酶- 1表达导致细胞迁移,这是减毒与IL-17预处理受体中和抗体和小干扰RNA金属蛋白酶- 1 (siRNA)。迁移也减弱了它的组织基质金属蛋白酶抑制剂(TIMP) 1。此外,p38增殖作用的蛋白质激酶抑制剂(SB203580)抑制(MAPK)IL-17A-induced迁移和增加金属蛋白酶- 1 upregulation PDL的成纤维细胞。p38 MAPK参与IL-17A-induced金属蛋白酶- 1进一步表达和细胞迁移证实了p38αsiRNA转染。核因子kappaB (NF -κB)抑制剂吡咯烷二硫代氨基甲酸()也抑制了细胞迁移和金属蛋白酶- 1表达增强IL-17A。抑制IL-17A-induced NF -κB核易位和NF -κB绑定活动。我们的研究结果表明,IL-17A增强了通过增加金属蛋白酶- 1 PDL成纤维细胞的迁移p38 MAPK表达通过IL-17受体,和NF -κB信号转导途径。

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