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首页> 外文期刊>Cellular immunology >The effect of ROCK on TNF-alpha-induced CXCL8 secretion by intestinal epithelial cell lines is mediated through MKK4 and JNK signaling
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The effect of ROCK on TNF-alpha-induced CXCL8 secretion by intestinal epithelial cell lines is mediated through MKK4 and JNK signaling

机译：ROCK通过MKK4和JNK信号传导介导小肠上皮细胞系对TNF-α诱导的CXCL8分泌的影响

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摘要

Intestinal epithelial cells (IEC) play a role in mucosal inflammatory responses by producing important chemokines like CXCL8 when stimulated by TNF-alpha. Previously, we found that IEC cell lines required the Rho-associated kinase, ROCK, for CXCL8 responses after IL-1 stimulation. This study extends these findings by showing that inhibiting ROCK suppressed TNF-alpha-induced CXCL8 secretion by Caco-2 and DLD1 colonic epithelial cell lines and CXCL8 mRNA levels in Caco-2 cells. RNAi knockdown experiments indicated that the inhibitory effect was mediated by ROCK2, and not ROCK1. Inhibiting ROCK had no effect on TNF-stimulated I kappa beta alpha phosphorylation and degradation or p38 MAPK phosphorylation indicating that ROCK plays no role in these signaling pathways. However, inhibiting ROCK suppressed TNF-induced phosphorylation of the p54 JNK isoform and phosphorylation of the upstream MKK4 kinase. These results suggest that ROCK is required for CXCL8 responses by TNF-stimulated IEC by affecting intracellular signaling through MKK4 and JNK. (C) 2015 Elsevier Inc. All rights reserved.
机译：肠上皮细胞（IEC）在受到TNF-α刺激时会产生重要的趋化因子（如CXCL8），从而在粘膜炎症反应中发挥作用。以前，我们发现IEC细胞系在IL-1刺激后需要Rho相关激酶ROCK来实现CXCL8反应。这项研究通过显示抑制ROCK抑制了Caco-2和DLD1结肠上皮细胞系以及Caco-2细胞中CXCL8 mRNA水平抑制TNF-α诱导的CXCL8分泌。 RNAi敲低实验表明抑制作用是由ROCK2，而不是ROCK1介导的。抑制ROCK对TNF刺激的Iκβ磷酸化和降解或p38 MAPK磷酸化没有影响，表明ROCK在这些信号传导途径中不起作用。但是，抑制ROCK可抑制TNF诱导的p54 JNK亚型的磷酸化和上游MKK4激酶的磷酸化。这些结果表明，ROCK通过TNF刺激的IEC通过影响细胞内通过MKK4和JNK的信号传导来实现CXCL8应答。 （C）2015 Elsevier Inc.保留所有权利。

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