Division of Gastrointestinal Surgery, Department of General Surgery, First Affiliated Hospital, Nanjing Medical University, Nanjing, China.
FEBS Lett. 2011 Oct 3;585(19):3113-9. doi: 10.1016/j.febslet.2011.08.045. Epub 2011 Sep 6.
AQP3 is a water/glycerol transporter expressed at the basolateral membrane of colonic epithelial cells. Although AQPs are expressed in the gastrointestinal tract, their effect on intestinal barrier has not been clear. Here, we showed that knockdown of AQP3 caused a dramatic, dose-dependent increase in E. coli C25 translocation, with the reduction of TEER and increasing LY permeability. Western blots revealed that expression of Claudin-1 and Occludin were significantly decreased in the AQP3 knockdown group, demonstrating that this treatment enhances paracellular permeability via an opening of the tight junction complex. These data not only describe the correlation between transcellular and paracellular pathways in human intestines, but also show that targeted knockdown of AQP3 might impair the intestinal barrier integrity.
AQP3 是一种水/甘油转运体，表达于结肠上皮细胞的基底外侧膜。尽管 AQPs 在胃肠道中表达，但它们对肠道屏障的影响尚不清楚。在这里，我们表明，AQP3 的敲低导致大肠杆菌 C25 的转运显著增加，呈剂量依赖性，TEER 降低，LY 通透性增加。Western blot 显示，AQP3 敲低组 Claudin-1 和 Occludin 的表达明显减少，表明这种处理通过开放紧密连接复合物增加了细胞旁通透性。这些数据不仅描述了人肠中细胞内和细胞旁途径之间的相关性，还表明靶向敲低 AQP3 可能损害肠道屏障的完整性。
