Pseudomonas aeruginosa quorum-sensing signaling molecule N-3-oxododecanoyl homoserine lactone induces matrix metalloproteinase 9 expression via the AP1 pathway in rat fibroblasts

Pseudomonas aeruginosa quorum-sensing signaling molecule N-3-oxododecanoyl homoserine lactone induces matrix metalloproteinase 9 expression via the AP1 pathway in rat fibroblasts
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铜绿假单胞菌群体感应信号分子N-3-氧代十二酰高丝氨酸内酯通过AP1途径诱导大鼠成纤维细胞基质金属蛋白酶9的表达

DOI:
10.1080/09168451.2015.1056509
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发表时间:
2015
期刊:
Biosci Biotechnol Biochem
影响因子:
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通讯作者:
Tsukasa Ikeda and Hiromi Sanada
Tsukasa Ikeda and Hiromi Sanada
中科院分区:
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文献类型:
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作者:
6.Gojiro Nakagami;Takeo Minematsu;Tomohiro Morohoshi;Takumi Yamane;Toshiki Kanazawa;Lijuan Huang;Mayumi Asada;Takashi Nagase;Shin-ichi Ikeda;Tsukasa Ikeda and Hiromi Sanada

文献摘要

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群体感应是一种细胞间的通讯机制,它负责调节许多细菌毒力因子和生物膜的成熟,因此在伤口感染的建立中起重要作用。群体感应信号可能诱发炎症,使伤口易受感染。然而,这种相互作用还没有得到很好的研究。我们检查了p的效果。群体感应信号n -3-氧-十二烷基高丝氨酸内酯(3OC12-HSL)对大鼠-1成纤维细胞基质金属蛋白酶(MMP) 9表达的影响。3OC12-HSL上调启动子区带有AP-1结合位点的themmp9基因的表达。结果表明,暴露于3OC12-HSL后,c-Fos基因表达迅速增加,c-Fos蛋白发生核易位;用AP-1抑制剂预处理后,这两种效果都减弱了。这些结果表明3OC12-HSL可以通过AP-1信号通路改变mmp9基因在成纤维细胞中的表达。
Quorum sensing is a cell-to-cell communication mechanism, which is responsible for regulating a number of bacterial virulence factors and biofilm maturation and therefore plays an important role for establishing wound infection. Quorum-sensing signals may induce inflammation and predispose wounds to infection byPseudomonas aeruginosa; however, the interaction has not been well investigated. We examined the effects of theP. aeruginosalas quorum-sensing signal, N-3-oxo-dodecanoyl homoserine lactone (3OC12-HSL), on matrix metalloproteinase (MMP) 9 expression in Rat-1 fibroblasts. 3OC12-HSL upregulated the expression of theMMP9gene bearing an activator protein-1 (AP-1) binding site in the promoter region. We further investigated the mechanism underlying this effect.c-Fosgene expression increased rapidly after exposure to 3OC12-HSL, and nuclear translocation of c-Fos protein was observed; both effects were reduced by pretreatment with an AP-1 inhibitor. These results suggest that 3OC12-HSL can alterMMP9gene expression in fibroblasts via the AP-1 signaling pathway.