Superinduction of NF-kappa B by actinomycin D and cycloheximide in epithelial cells.
Superinduction of NF-kappa B by actinomycin D and cycloheximide in epithelial cells.
复制标题
上皮细胞中放线菌酮和放线菌素对 NF-κ B 的超诱导作用。
DOI：
10.1006/bbrc.1996.0093
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发表时间：
1996
影响因子：
3.1
通讯作者：
P. Barnes
中科院分区：
文献类型：
--
作者：
R. Newton;I. Adcock;P. Barnes
上皮细胞积极参与炎症，并在哮喘等炎性疾病中发挥作用。在气道上皮中表达的许多促炎基因受转录因子NF-κ B的调节。我们发现，促炎细胞因子，IL-1 β和TNF α，以及蛋白激酶C激活剂导致NF-κ B B激活A549上皮细胞。该观察结果与NF-κ B在炎症中的主要作用一致。我们还表明，IL-1 β与蛋白质合成抑制剂，放线菌酮，或转录阻断剂，放线菌素D，共刺激的结果在超诱导NF-κ B，但不是转录因子Oct 1，AP-1，和Sp-1。我们推测，这可能是由于缺乏从头合成的NF-κ B抑制剂，I κ B α，并建议，这种现象可能有助于解释广泛观察到的效果的mRNA超诱导的主要反应基因的翻译阻断剂。
Epithelial cells are actively involved in inflammation and play a role in inflammatory diseases such as asthma. Numerous proinflammatory genes, expressed in the airway epithelium, are regulated by the transcription factor NF-kappa B. We show that the proinflammatory cytokines, IL-1 beta and TNF alpha, as well as a protein kinase C activator cause NF-kappa B activation in A549 epithelial cells. This observation is consistent with a major role for NF-kappa B in inflammation. We also demonstrate that IL-1 beta costimulation with a protein synthesis inhibitor, cycloheximide, or a transcription blocker, actinomycin D, results in superinduction of NF-kappa B but not the transcription factors Oct 1, AP-1, and Sp-1. We speculate that this may be due to lack of de novo synthesis of the NF-kappa B inhibitor, I kappa B alpha, and suggest that this phenomena may help explain the widely observed effect of mRNA superinduction of primary response genes in response to translational blockers.