Oxidation of thiols and modification of redox-sensitive signaling in human lung epithelial cells exposed to Pseudomonas pyocyanin.
Oxidation of thiols and modification of redox-sensitive signaling in human lung epithelial cells exposed to Pseudomonas pyocyanin.
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暴露于绿脓杆菌的人肺上皮细胞中硫醇的氧化和氧化还原敏感信号的修饰。
DOI：
10.1080/15287394.2010.514233
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Abdalla,MaherY
中科院分区：
文献类型：
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作者：
Ahmad,ImanM;Britigan,BradleyE;Abdalla,MaherY
本研究的目的是研究pyocyanin暴露对A549和HBE细胞系线粒体GSH、其他细胞硫醇（thioredoxin-1, Trx-1）和氧化敏感信号通路缺氧诱导因子（HIF-1α）和血红素加氧酶（HO-1）的影响。用铜绿假单胞菌提取的不同浓度的pyocyanin处理A549人II型肺泡上皮细胞和人支气管上皮细胞。测定细胞质和线粒体硫醇和氧化敏感信号转导蛋白（HIF-1α和HO-1）。暴露于花青素在细胞线粒体中产生活性氧（ROS）并改变细胞总谷胱甘肽（GSH）。在体内条件下，Pyocyanin在A549人II型肺泡上皮细胞和HBE细胞中的氧化Trx-1分别增加了184和74%。氧化线粒体谷胱甘肽（GSSG）在两种细胞类型中升高两倍以上。Pyocyanin还增加了细胞氧化敏感蛋白HIF-1α和HO-1。数据表明，花青素诱导的线粒体和细胞质硫醇以及氧化敏感蛋白的改变可能与toP有关。铜绿杆菌介导的肺损伤。
The aim of this study was to examine the effects of pyocyanin exposure on mitochondrial GSH, other cellular thiols (thioredoxin-1, Trx-1), and oxidant-sensitive signaling pathways hypoxia inducible factor (HIF-1α) and heme oxygenase (HO-1) in A549 and HBE cell lines. A549 human type II alveolar epithelial cells and human bronchial epithelial (HBE) cells were treated with varying concentrations of pyocyanin extracted fromPseudomonas aeruginosabacteria. Cytoplasmic and mitochondrial thiols and oxidant sensitive signal transduction proteins (HIF-1α and HO-1) were measured. Exposure to pyocyanin generated reactive oxygen species (ROS) in cellular mitochondria and altered total cellular glutathione (GSH). Pyocyanin, at concentrations present in conditions in vivo, increased oxidized Trx-1 in A549 human type II alveolar epithelial cells and HBE cells by 184 and 74%, respectively. Oxidized mitochondrial glutathione (GSSG) was elevated more than twofold in both cell types. Pyocyanin also increased the cellular oxidant-sensitive proteins HIF-1α and HO-1. Data indicate that pyocyanin-induced alterations in mitochondrial and cytosolic thiols, as well as oxidant-sensitive proteins, may contribute toP. aeruginosa-mediated lung injury.