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Loss of C/EBPδ enhances apoptosis of intestinal epithelial cells and exacerbates experimental colitis in mice
Author(s) -
Jozawa Hiroki,
InoueYamauchi Akane,
Arimura Sumimasa,
Yamanashi Yuji
Publication year - 2019
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12711
Subject(s) - colitis , apoptosis , inflammatory bowel disease , inflammation , ulcerative colitis , knockout mouse , biology , immunology , cancer research , ccaat enhancer binding proteins , transcription factor , medicine , pathology , disease , receptor , dna binding protein , biochemistry , gene
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.