Interleukin-13 promotes expression of Alix to compromise renal tubular epithelial barrier function.
The epithelial barrier dysfunction plays a critical role in a number of kidney diseases. The mechanism is unclear. Alix is a protein involving in protein degradation in epithelial cells. This study aims to investigate that interleukin (IL)-13 inhibits Alix to compromise the kidney epithelial barrier function. In this study, the murine collecting duct cell line (M-1) was cultured in Transwell inserts to investigate the significance of Alix in compromising the epithelial barrier functions. T cell (Teff cells) proliferation assay was employed to assess the antigenicity of ovalbumin (OVA) that was transported across the M-1 monolayer barrier. The results showed that M-1 cells express Alix. Exposure to interleukin (IL)-13 markedly decreased the expression of Alix in M-1 cells, which compromised the M-1 monolayer barrier functions by showing the increases in the permeability to OVA. Over-expression of Alix abolished the IL-13-induced M-1 monolayer barrier dysfunction. Knockdown of Alix significantly increased M-1 monolayer permeability. The OVA collected from the Transwell basal chambers induced the OVA-specific T cell proliferation. We conclude that IL-13 compromises M-1 epithelial barrier functions via inhibiting Alix expression.
['Xu|Chen|C|', 'Sun|Guangdong|G|', 'Yang|Jie|J|', 'Sun|Qianmei|Q|', 'Tong|Zhaohui|Z|']
D000818:Animals D002135:Calcium-Binding Proteins D002463:Cell Membrane Permeability D002478:Cells, Cultured D017097:Electric Impedance D004847:Epithelial Cells D018793:Interleukin-13 D007684:Kidney Tubules D051379:Mice D010047:Ovalbumin D015854:Up-Regulation D019459:Urothelium
barrier function kidney epithelial cells biological transport renal tubules