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首页> 外文期刊>Life sciences >Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells
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Difructose anhydride III and sodium caprate activate paracellular transport via different intracellular events in Caco-2 cells

机译：果糖酐III和癸酸钠通过Caco-2细胞中不同的细胞内事件激活细胞旁运输

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A nondigestible disaccharide, difiructose anhydride (DFA) III, is known to activate calcium transport via tight junctions (TJs); however, the characteristics of and mechanisms for the increase in paracellular transport induced by DFAIII have not been clarified. We compared the effect of DFAIII with that of sodium caprate (C10), a well-known enhancer of TJ permeability, on the changes in TJ proteins, transport of paracellular markers, and effects of nine cellular signaling blockers using Caco-2 monolayers. The addition of DFAIII (0-100 mmol/L) and C10 (0-10 mmol/L) to the apical medium of the Caco-2 monolayers dose-dependently decreased transepithelial electrical resistance (TER), which is an indicator of TJ permeability. The reduction with C10 was much faster than that with DFAIII. Transport of the paracellular markers of various molecular weights (182-43,200) was elevated by the addition of 100 mmol/L DFAIII and 10 mmol/L C10. The transport rates were much in the presence of C10 than of DFAIII, while the reduction in TER by two treatments was similar (from 1000 to 300 Omega cm(2)). Treatment with DFAIII and C10 changed the distribution of actin filament and claudin-1, but not occludin, junctional adhesion molecule-1, or zonula occludens-1; however, alterations in the patterns of the TJ proteins differed according to treatment. An inhibitor of myosin light chain kinase and a chelator of intracellular calcium ion ([Ca2+](i)) attenuated the TER reduction by C10, but not by DFAIII. These data demonstrate that the increase in TJ permeability induced by DFAIII results from the alterations to actin and claudin-1 via [Ca2+](i)-independent mechanisms. (c) 2006 Elsevier Inc. All rights reserved.
机译：已知一种不易消化的二糖，二果糖酐（DFA）III通过紧密连接（TJ）激活钙的转运。然而，尚不清楚DFAIII诱导的旁细胞运输增加的特征和机制。我们将DFAIII与著名的TJ通透性增强剂癸酸钠（C10）的效果进行了比较，比较了TJ蛋白的变化，旁细胞标志物的转运以及使用Caco-2单层的九种细胞信号传导阻滞剂的效果。在Caco-2单层的根尖介质中添加DFAIII（0-100 mmol / L）和C10（0-10 mmol / L）剂量依赖性降低跨上皮电阻（TER），这是TJ渗透性的指标。 C10的还原比DFAIII的还原快得多。通过添加100 mmol / L DFAIII和10 mmol / L C10，提高了各种分子量（182-43,200）副细胞标志物的转运。有C10的情况下的转运速度要比DFAIII大得多，而两种处理方法对TER的减少是相似的（从1000到300 Omega cm（2））。用DFAIII和C10处理可改变肌动蛋白丝和claudin-1的分布，但不会改变闭合蛋白，连接黏附分子1或小带闭合蛋白1的分布。然而，TJ蛋白模式的改变根据治疗而不同。肌球蛋白轻链激酶抑制剂和细胞内钙离子螯合剂（[Ca2 +]（i））通过C10而不是DFAIII减弱TER的降低。这些数据表明，由DFAIII诱导的TJ通透性增加是由于经由[Ca2 +]（i）无关的机制改变为肌动蛋白和claudin-1。 （c）2006 Elsevier Inc.保留所有权利。

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