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首页> 外文期刊>American Journal of Physiology >Activation of the EGF receptor signaling pathway in airway epithelial cells exposed to Utah Valley PM.
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Activation of the EGF receptor signaling pathway in airway epithelial cells exposed to Utah Valley PM.

机译：EGF受体信号通路在暴露于犹他谷PM的气道上皮细胞中的激活。

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摘要

Exposure to ambient particulate matter (PM) in the Utah Valley has previously been associated with a variety of adverse health effects. To investigate intracellular signaling mechanisms for pulmonary responses to Utah Valley PM inhalation, human primary airway epithelial cells were exposed to aqueous extracts of PM collected from the year before (Y1), during (Y2), and after (Y3) the closure of a local steel mill located in the Utah Valley in this study. Transfection with kinase-deficient extracellular signal-regulated kinase (ERK) 1 constructs partially blocked Utah Valley PM-induced interleukin (IL)-8 promoter reporter activity. The mitogen-activated protein kinase/ERK kinase (MEK) activity inhibitor PD-98059 significantly abolished IL-8 released in response to Utah Valley PM, as did the epidermal growth factor (EGF) receptor kinase inhibitor AG-1478. Western blotting showed that Utah Valley PM induced phosphorylation of EGF receptor tyrosine, MEK1/2, and ERK1/2, which could be ablated with AG-1478 orPD-98059. For all findings, the potency of Utah Valley PM collected during Y2 was found to be lower relative to that of Y1 and Y3. These data demonstrate that Utah Valley PM can induce IL-8 expression partially through the activation of the EGF receptor signaling.
机译：以前，在犹他州山谷中暴露于环境颗粒物（PM）与各种不良健康影响有关。为了研究肺对犹他州谷粉吸入的肺反应的细胞内信号传导机制，将人原代气道上皮细胞暴露于从局部封闭前一年（Y1），期间（Y2）和之后（Y3）收集的PM的水提取物。这项研究位于犹他州山谷的一家钢铁厂。激酶缺陷型细胞外信号调节激酶（ERK）1构建体的转染部分阻断了犹他谷PM诱导的白介素（IL）-8启动子报道基因活性。有丝分裂原激活的蛋白激酶/ ERK激酶（MEK）活性抑制剂PD-98059与表皮生长因子（EGF）受体激酶抑制剂AG-1478一样，废除了响应于犹他谷PM释放的IL-8。蛋白质印迹表明，犹他州谷地PM诱导EGF受体酪氨酸，MEK1 / 2和ERK1 / 2的磷酸化，可被AG-1478或PD-98059消除。对于所有发现，发现Y2期间收集的犹他谷PM的效力相对于Y1和Y3较低。这些数据表明，犹他谷PM可以通过EGF受体信号传导的激活部分诱导IL-8表达。

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