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首页> 外文期刊>Journal of Cellular Physiology >Tumor Necrosis Factor- Increases Claudin-1, 4, and 7 Expression in Tubular Cells: Role in Permeability Changes
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Tumor Necrosis Factor- Increases Claudin-1, 4, and 7 Expression in Tubular Cells: Role in Permeability Changes

机译：肿瘤坏死因子-增加Claudin-1 47在管状细胞表达:作用渗透率的变化

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Tumor necrosis factor- (TNF), is a pathogenic cytokine in kidney disease that alters expression of claudins in tubular cells. Previously we showed that in LLC-PK1 cells TNF caused a biphasic change in transepithelial resistance (TER) consisting of an early drop and recovery, followed by a late increase. However, the underlying mechanisms and the role of specific claudins in the TER effect remained incompletely understood. Here we sought to define how TNF affects claudins 1, 4, and 7 in tubular cells and to correlate their changes with the TER effect. We show that TNF elevates total and surface levels of Cldn-1, 4, and 7, and increases their mRNA expression through the ERK and JNK pathways. Further, JNK is also important for TNF-induced changes in claudin-2 expression. Continuous monitoring of TER using Electric cell-substrate impedance sensing (ECIS) reveals that the two phases of the TNF effect are differently regulated. Specifically, inhibition of the ERK or JNK pathways prevent the late TER increase, but not the early TER effect. Silencing experiments also show that Cldn-1 is necessary for the early TNF-induced TER change, while all three claudins appear to contribute to the late TER increase. In summary, we define a central role for ERK and JNK in TNF-induced altered claudin expression and barrier tightening. Together, our current and previous works show that the TNF-induced early TER effect requires claudin-1, while claudin-2 decrease is a significant mediator of the late TER increase, and elevation in claudin-1, 4, and 7 contribute to a smaller extent. J. Cell. Physiol. 232: 2210-2220, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：肿瘤坏死因子(TNF)是一种致病性细胞因子在肾脏疾病改变表达式claudins的管状细胞。表明在LLC-PK1细胞肿瘤坏死因子引起两相的transepithelial阻力的变化(三)组成的一个早期下降和恢复,其次是后期增加。底层机制和具体的角色claudins TER效果仍不完全理解。影响claudins 1、4和7的管状细胞关联与内涵的变化效果。我们表明TNF提升和表面水平的Cldn-1 4和7,增加他们的通过ERK和物通路mRNA的表达。此外,TNF-induced物也很重要claudin-2表达的变化。监控额,使用电动的细胞基质通性阻抗传感显示,这两个概念阶段的肿瘤坏死因子的影响是不同的监管。物途径防止后期TER增加,但是没有早期的后效应。还表明,Cldn-1早期是必要的TNF-induced TER改变,而这三个claudins似乎有助于后期的增加。总结,我们定义了一个核心作用ERK和物在TNF-induced claudin表达和改变紧缩的障碍。先前的工作表明,TNF-induced早后效果需要claudin-1, claudin-2末的减少是一个重要的中介增加后,海拔claudin-1 47为一个更小的程度。杂志。232:2210 - 2220年,2017年。期刊、公司。

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