ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions

Endoplasmic reticulum stress is closely associated with the onset and progression of inflammatory bowel disease. ERdj5 is an endoplasmic reticulum-resident protein disulfide reductase that mediates the cleavage and degradation of misfolded proteins. Although ERdj5 expression is significantly higher in the colonic tissues of patients with inflammatory bowel disease than in healthy controls, its role in inflammatory bowel disease has not yet been reported. Hence, in the current study, we utilized ERdj5-knockout mice to investigate the potential roles of ERdj5 in inflammatory bowel disease. ERdj5 deficiency causes severe inflammation in mouse colitis models and weakens gut barrier function by increasing NF-κB-mediated inflammation. ERdj5 may not be indispensable for goblet cell function under steady-state conditions, while its deficiency induces goblet cell apoptosis under inflammatory stimuli. 8-week-old female ERdj5 KO mice and their corresponding WT mice were administered 2% DSS in drinking water for 5 days. Mice were sacrificed, RNA from colon tissues were isolated for RNA-seq analysis. Each groups contain 2-3 replicates.