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首页> 外文期刊>Journal of Cellular Physiology >Hyperoxia induces Egr-1 expression through activation of extracellular signal-regulated kinase 1/2 pathway.
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Hyperoxia induces Egr-1 expression through activation of extracellular signal-regulated kinase 1/2 pathway.

机译：通过氧过多诱发Egr-1表达式激活细胞外signal-regulated激酶1/2通路。

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摘要

Early growth response gene (Egr-1) is a stress response gene activated by various forms of stress and growth factor signaling. We report that supraphysiologic concentrations of O(2) (hyperoxia) induced Egr-1 mRNA and protein expression in cultured alveolar epithelial cells, as well as in mouse lung in vivo. The contribution of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK), p38 MAPK and PI3-kinase pathways to the activation of Egr-1 in response to hyperoxia was examined. Exposure to hyperoxia resulted in a rapid phosphorylation of ERK 1/2 kinases in mouse alveolar epithelial cells LA4. MEK inhibitor PD98059, but not inhibitors of p38 MAPK or PI3-kinase pathway, prevented Egr-1 induction by hyperoxia. The signaling cascade preceding Egr-1 activation was traced to epidermal growth factor receptor (EGFR) signaling. Hyperoxia is used as supplemental therapy in some diseases and typically results in elevated levels of reactive oxygen intermediates (ROI) in manylung cell types, the organ that receives highest O(2) exposure. Our results support a pathway for the hyperoxia response that involves EGF receptor, MEK/ERK pathway, and other unknown signaling components leading to Egr-1 induction. This forms a foundation for analysis of detailed mechanisms underlying Egr-1 activation during hyperoxia and understanding its consequences for regulating cell response to oxygen toxicity. J. Cell. Physiol. 196: 326-333, 2003.
机译：早期生长反应基因(Egr-1)是一种压力通过各种形式的响应基因激活压力和生长因子信号。supraphysiologic浓度的O (2)(氧过多)诱导Egr-1信使rna和蛋白质在培养的肺泡上皮细胞中表达,以及在老鼠体内肺。增殖作用的贡献激酶激酶(MEK) /细胞外signal-regulated激酶(ERK), p38 MAPK和pi3激酶通路的激活Egr-1对氧过多。氧过多导致快速的磷酸化在小鼠肺泡上皮细胞ERK激酶1/2细胞LA4。p38 MAPK的抑制剂或pi3激酶通路,通过氧过多阻止Egr-1感应。信号级联前Egr-1激活追溯到表皮生长因子受体(EGFR)信号。治疗一些疾病,通常的结果高浓度的活性氧中间体(ROI)在manylung细胞,器官收到最高O(2)接触。支持氧过多反应的途径涉及EGF受体,MEK / ERK通路,和其他导致Egr-1未知信号组件归纳。Egr-1详细的机制激活期间氧过多和理解它影响调节细胞反应氧中毒。2003.

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