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首页> 外文期刊>American Journal of Physiology >PKC-pl isoform activation is required for EGF-induced NF-KB inactivation and IkBa stabilization and protection of F-actin assembly and barrier function in enterocyte monolayers
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PKC-pl isoform activation is required for EGF-induced NF-KB inactivation and IkBa stabilization and protection of F-actin assembly and barrier function in enterocyte monolayers

机译：EGF诱导的NF-KB失活和IkBa稳定以及保护F-肌动蛋白装配和肠单层细胞屏障功能需要PKC-pl亚型激活

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摘要

Using monolayers of intestinal Caco-2 cells, we reported that activation of NF-KB is required for oxidative disruption and that EGF protects against this injury but the mechanism remains unclear. Activation of the PKC-beta_1 isoform is key to monolayer barrier integrity. We hypothesized that EGF-induced activation of PKC-beta_1 prevents oxidant-induced activation of NF-KB and the consequences of NF-KB activation, F-actin, and barrier dysfunction. We used wild-type (WT) and transfected cells. The latter were transfected with varying levels of cDNA to overex-press or underexpress PKC-beta1.
机译：使用单层的肠Caco-2细胞，我们报道了NF-KB的激活是氧化破坏所必需的，而EGF可以防止这种损伤，但其机制尚不清楚。 PKC-beta_1同工型的激活是单层屏障完整性的关键。我们假设EGF诱导的PKC-beta_1的激活阻止了氧化剂诱导的NF-KB的激活以及NF-KB激活，F-肌动蛋白和屏障功能障碍的后果。我们使用野生型（WT）和转染的细胞。后者用不同水平的cDNA转染，以过度表达或表达不足PKC-beta1。

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