کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2048641 | 1074086 | 2011 | 7 صفحه PDF | دانلود رایگان |

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.
► We interfere AQP3 expression in Caco-2 cell line.
► We examine tight junction proteins, TEER, LY permeability and bacterial translocation.
► TEER, expressing of Claudin-1 and Occludin are decreased in AQP3 knockdown group.
► Bacterial translocation and LY permeability are increased in AQP3 knockdown group.
► Targeted knockdown of AQP3 might impair the intestinal barrier integrity.
Journal: FEBS Letters - Volume 585, Issue 19, 3 October 2011, Pages 3113–3119