Inflammatory Bowel Disease Susceptibility Gene C1ORF106 Regulates Intestinal Epithelial Permeability
2018
Intestinal epithelial cells form a physical barrier that is tightly regulated to control
intestinal permeability.
Proinflammatory cytokines, such as TNF-α, increase epithelial permeability through disruption of epithelial junctions. The regulation of the epithelial barrier in inflammatory gastrointestinal disease remains to be fully characterized. In this article, we show that the human
inflammatory bowel diseasegenetic susceptibility gene C1ORF106 plays a key role in regulating gut epithelial permeability. C1ORF106 directly interacts with cytohesins to maintain functional epithelial
cell junctions. C1orf106 -deficient mice are hypersensitive to TNF-α–induced increase in epithelial permeability, and this is associated with increased diarrhea. This study identifies C1ORF106 as an epithelial
cell junctionprotein, and the loss of C1ORF106 augments TNF-α–induced intestinal epithelial leakage and diarrhea that may play a critical role in the development of
inflammatory bowel disease.
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