Journal
PATHOLOGY RESEARCH AND PRACTICE
Volume 214, Issue 2, Pages 245-252Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.prp.2017.11.004
Keywords
Crohn's disease; Intestinal epithelial cells; Apoptosis; Runx2; p53
Categories
Funding
- National Natural Science Foundation of China [81401365, 81300955]
- Nantong Science and Technology Innovation Project [MS12015056, HS2013014, BK2012075, BK2011013]
- 14th Six Talents Peak Project of Jiangsu Province [SWYY-058]
- Priority Academic Program of Jiangsu Higher Education Institutions (PAPD)
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Apoptosis in intestinal epithelial cells (IECs) prevents the development of Crohn's disease (CD), a type of inflammatory bowel disease (IBD). Runt-related transcription factor 2 (Runx2) inhibits apoptosis in osteosarcoma-derived U2OS cells via down-regulating the transcriptional activity of p53. However, the expression and function of Runx2 in CD remain unclear. In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. In a TNF-alpha-treated HT29 cell colitis model, the down-regulation of Runx2 was accompanied by the up-regulation of apoptotic markers, including cleaved caspase-3 and Bax. Furthermore, Runx2 overexpression effectively decreased TNF-alpha-induced Bax and cleaved caspase-3 expression levels. In conclusion, our data indicated that Runx2 might protect IECs from apoptosis in CD, thus revealing a novel molecular target for treating CD.
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