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Loss of C/EBPδ enhances apoptosis of intestinal epithelial cells and exacerbates experimental colitis in mice.

Authors
  • Jozawa, Hiroki1
  • Inoue-Yamauchi, Akane1
  • Arimura, Sumimasa1
  • Yamanashi, Yuji1
  • 1 Division of Genetics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. , (Japan)
Type
Published Article
Journal
Genes to Cells
Publisher
Wiley (Blackwell Publishing)
Publication Date
Sep 01, 2019
Volume
24
Issue
9
Pages
619–626
Identifiers
DOI: 10.1111/gtc.12711
PMID: 31233664
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Inflammatory bowel diseases (IBDs) are characterized by chronic inflammation involving intestinal tissue damage, which include ulcerative colitis and Crohn's disease as major entities. Accumulating evidence suggests that excessive apoptosis of intestinal epithelial cells (IECs) contributes to the development of IBD. It was recently reported that the transcription factor CCAAT/enhancer-binding protein delta (C/EBPδ) is involved in inflammation; however, its role in colitis remains unclear. Here, we found that C/EBPδ knockout mice showed enhanced susceptibility to dextran sodium sulfate (DSS)-induced colitis, a mouse model of IBD, which was associated with severe colonic inflammation and mucosal damage with increased IEC apoptosis. Additionally, DSS stimulation induced increased expression of pro-apoptotic BH3-only protein Bim in the colon of C/EBPδ knockout mice. Collectively, our findings demonstrate that C/EBPδ plays an essential role in suppressing DSS-induced colitis, likely by attenuating IEC apoptosis. © 2019 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd.

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