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首页> 外文期刊>American Journal of Physiology >Neutrophil elastase induces IL-8 gene transcription and protein release through p38/NF-{kappa}B activation via EGFR transactivation in a lung epithelial cell line.
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Neutrophil elastase induces IL-8 gene transcription and protein release through p38/NF-{kappa}B activation via EGFR transactivation in a lung epithelial cell line.

机译：中性粒细胞弹性蛋白酶通过肺上皮细胞系中的EGFR反式激活通过p38 / NF- {kappa} B激活诱导IL-8基因转录和蛋白质释放。

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摘要

In this study, we investigated the regulation and mechanism of IL-8 expression by A549 human lung carcinoma cells treated with neutrophil elastase (NE). NE-treated cells exhibited significantly higher IL-8 protein levels in culture media compared with cells treated with vehicle alone. Blocking of gene transcription with actinomycin D suggested that NE stimulated IL-8 synthesis via increased mRNA expression, which was verified by real-time RT-PCR. NE activated the IL-8 promoter but did not alter the stability of its mRNA, confirming that the protease induced IL-8 synthesis through increased gene transcription. The results from the use of chemical inhibitors and mutant gene constructs against various signal transduction components seem to suggest the linear signaling pathway involving the activation of PKC-delta --> dual oxidase 1 --> reactive oxygen species --> TNF-alpha-converting enzyme --> EGF receptor --> p38 --> NF-kappaB for NE-activated IL-8 gene expression. A NF-kappaB potential binding site, located between nucleotides -82 and -69 of the IL-8 promoter, was identified as necessary for NE-induced IL-8 transcription. We conclude that NE increases IL-8 transcription through p38/NF-kappaB activation via EGFR transactivation.
机译：在这项研究中，我们研究了中性粒细胞弹性蛋白酶（NE）处理的A549人肺癌细胞对IL-8表达的调控及其机制。与单独用媒介物处理的细胞相比，经NE处理的细胞在培养基中表现出明显更高的IL-8蛋白水平。用放线菌素D阻断基因转录表明NE通过增加的mRNA表达刺激了IL-8的合成，这已被实时RT-PCR证实。 NE激活了IL-8启动子，但没有改变其mRNA的稳定性，从而证实蛋白酶通过增加基因转录来诱导IL-8合成。使用化学抑制剂和突变基因构建体对抗各种信号转导成分的结果似乎表明线性信号通路涉及PKC-δ激活->双氧化酶1->活性氧->TNF-α-转化酶-> EGF受体-> p38->NF-κB用于NE激活的IL-8基因表达。鉴定出位于IL-8启动子的核苷酸-82和-69之间的NF-κB潜在结合位点是NE诱导的IL-8转录所必需的。我们得出结论，NE通过EGFR反式激活通过p38 / NF-kappaB激活增加IL-8转录。

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