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Jeong Hyunjin,Hong Eun-Hye,Ahn Jae-Hee,Cho Jaewon,Jeong Jae-Hyeon,Kim Chae-Won,Yoon Byung-Il,Koo Ja Hyun,Park Yun-Yong,Yang Yoon Mee,Iwawaki Takao,Bruce A. Vallance,Chang Sun-Young,Ko Hyun-Jeong 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
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. In the current study, we used 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, but its deficiency induces goblet cell apoptosis under inflammatory conditions. Treatment of ERdj5-knockout mice with the chemical chaperone ursodeoxycholic acid ameliorated severe colitis by reducing endoplasmic reticulum stress. These findings highlight the important role of ERdj5 in preserving goblet cell viability and function by resolving endoplasmic reticulum stress.