作者: Guillermo Ares , Christie Buonpane , John Sincavage , Carrie Yuan , Douglas R. Wood
DOI: 10.1038/S41598-019-41442-4
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摘要: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal emergency of neonates. Epithelial tight junction (TJ) proteins, such as claudins, are essential for regulation and function the intestinal barrier. Rho kinase (ROCK) affects cellular permeability TJ regulation. We hypothesized that protein changes would correlate with increased in experimental NEC, ROCK inhibitors be protective against NEC by key claudin proteins. tested this hypothesis using an vivo rat pup model, vitro model human samples from patients without NEC. Experimental was induced rats via hypoxia bacteria-containing formula, Caco-2 cells media inoculated LPS. The expression claudins measured gene analysis. pups had compared to controls. Gene 2 Sub-cellular fractionation localized cytoskeleton. inhibition associated normalization these alterations decreased severity Co-immunoprecipitation caveolin-1 suggests may act shuttle internalization seen In conclusion, 2, binding trafficking