Intestinal epithelial cell (IEC) apoptosis plays a vital role in the pathogenesis of Crohn's disease (CD), which is an inflammatory bowel disease (IBD). Activating transcription factor 3 (ATF3) modulates apoptosis under stress via regulating the p53 pathway. However, the expression and function of ATF3 in CD are unclear. In the present study, ATF3, p53, and p53 target gene Bax expression increased in CD patients; a mouse 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced CD model; and a TNF-α-treated HT29 cell colitis model. ATF3 knockdown effectively decreased TNF-α-induced p53 and Bax expression, as well as inhibited the apoptosis of HT29 cells. Additionally, ATF3 enhanced the stability and transcription activity of p53 via interacting with p53. In summary, these data indicated that ATF3 might promote IEC apoptosis in CD via up-regulating the stability and transcription activity of p53, implying a novel molecular target for CD therapy.
Activating transcription factor 3 promotes intestinal epithelial cell apoptosis in Crohn's disease.
Liugen Gu,Zhenming Ge,Yamin Wang,M. Shen,Ping Zhao
Published 2018 in Pathology, Research and Practice
ABSTRACT
PUBLICATION RECORD
- Publication year
2018
- Venue
Pathology, Research and Practice
- Publication date
2018-06-01
- Fields of study
Biology, Medicine, Chemistry
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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