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:
影响因子:
--
通讯作者:
Tsukasa Ikeda and Hiromi Sanada
中科院分区:
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
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.