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首页> 外文期刊>Cell and Tissue Research >TNFα up-regulates claudin-2 expression in epithelial HT-29/B6 cells via phosphatidylinositol-3-kinase signaling
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TNFα up-regulates claudin-2 expression in epithelial HT-29/B6 cells via phosphatidylinositol-3-kinase signaling

机译：TNFα通过磷脂酰肌醇3激酶信号传导上调HT-29 / B6细胞中claudin-2的表达

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摘要

Our aim has been to characterize the molecular mechanisms regulating the expression of the channel-forming tight-junctional protein claudin-2 in response to the pro-inflammatory cytokine tumor necrosis factor-α (TNFα), which is elevated, for example, in active Crohn’s disease. TNFα caused an 89% decrease of the paracellular resistance in colonic HT-29/B6 cells, whereas transcellular resistance was unaltered. The claudin-2 protein level was increased by TNFα without changes in subcellular tight-junctional protein localization as revealed by confocal laser scanning microscopy. Enhanced gene expression was identified as the source of this increase, since claudin-2-specific mRNA and promoter activity was elevated, whereas mRNA stability remained unaltered. Specific inhibitors and phospho-specific antibodies revealed that the increased gene expression of claudin-2 after TNFα treatment was mediated by the phosphatidylinositol-3-kinase pathway. Thus, the up-regulation of claudin-2 by TNFα is attributable to the regulation of the expression of the gene, as a result of which epithelial barrier function is disturbed, for example, during chronic intestinal inflammation.
机译：我们的目标是表征响应促炎性细胞因子肿瘤坏死因子-α（TNFα）（例如，在活跃状态下升高）而调节通道形成紧密连接蛋白claudin-2表达的分子机制。克罗恩病。 TNFα导致结肠HT-29 / B6细胞的副细胞抗性降低89％，而跨细胞抗性未改变。共聚焦激光扫描显微镜显示，TNFα可增加claudin-2蛋白的水平，而亚细胞紧密连接蛋白的定位不变。基因表达的增强被认为是这种增加的原因，因为claudin-2特异性mRNA和启动子活性提高了，而mRNA的稳定性保持不变。特异性抑制剂和磷酸化特异性抗体显示，TNFα处理后claudin-2的基因表达增加是由磷脂酰肌醇-3-激酶途径介导的。因此，TNFα对claudin-2的上调可归因于基因表达的调节，其结果是，例如在慢性肠道炎症期间，上皮屏障功能受到干扰。

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