| First Author | Jozawa H | Year | 2019 |
| Journal | Genes Cells | Volume | 24 |
| Issue | 9 | Pages | 619-626 |
| PubMed ID | 31233664 | Mgi Jnum | J:295529 |
| Mgi Id | MGI:6453924 | Doi | 10.1111/gtc.12711 |
| Citation | Jozawa H, et al. (2019) Loss of C/EBPdelta enhances apoptosis of intestinal epithelial cells and exacerbates experimental colitis in mice. Genes Cells 24(9):619-626 |
| abstractText | 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/EBPdelta) is involved in inflammation; however, its role in colitis remains unclear. Here, we found that C/EBPdelta 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/EBPdelta knockout mice. Collectively, our findings demonstrate that C/EBPdelta plays an essential role in suppressing DSS-induced colitis, likely by attenuating IEC apoptosis. |
