한빛사논문
Hyunjin Jeong1,2,10, Eun-Hye Hong1,10, Jae-Hee Ahn1,2, Jaewon Cho1,2, Jae-Hyeon Jeong1,2, Chae-Won Kim1,2, Byung-Il Yoon3, Ja Hyun Koo4, Yun-Yong Park5, Yoon Mee Yang1,2, Takao Iwawaki6, Bruce A. Vallance7, Sun-Young Chang8 and Hyun-Jeong Ko1,9
1Department of Pharmacy, Kangwon National University, Chuncheon 24341, Republic of Korea.
2KNU Researcher training program for developing Anti-Viral Innovative Drugs (BK21 plus), Kangwon National University, Chuncheon 24341, Republic of Korea.
3College of Veterinary Medicine, Kangwon National University, Chuncheon 24341, Republic of Korea.
4College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
5Department of Life Science, Chung-Ang University, Seoul 06974, Republic of Korea.
6Division of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University, Uchinada 920-0293, Japan.
7BC Children’s Hospital Research Institute, University of British Columbia, Vancouver, BC, Canada.
8College of Pharmacy, Ajou University, Suwon 16499, Republic of Korea.
9Global/Gangwon Innovative BiologicsRegional Leading Research Center (GIB-RLRC), Kangwon National University, Chuncheon 24341, Republic of Korea.
10These authors contributed equally: Hyunjin Jeong, Eun-Hye Hong.
Corresponding authors : Correspondence to Sun-Young Chang or Hyun-Jeong Ko.
Abstract
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.
논문정보
관련 링크
연구자 키워드
관련분야 연구자보기
관련분야 논문보기