Abstract |
Apoptosis in intestinal epithelial cells (IECs) promotes the development of ulcerative colitis (UC), a type of inflammatory bowel disease (IBD). Efficient clearance of apoptotic cells is essential for tissue homeostasis in metazoans. Actin related protein 3 (ARP3) promotes endothelial dysfunction. The expression and function of ARP3 in UC remains unclear. In this study, the expression of apoptotic markers as p53, Bax, Cleaved-Caspease9 and Cleaved-Caspease3 were proved to be increased in the intestinal epithelial cells (IECs) of UC patients and in a mouse disuccinimidyl suberate(DSS)-induced colitis model; meanwhile, ARP3 expression was elevated. ARP3 expression levels and the severity of symptoms in patients with UC were positively correlated. By knocking down ARP3 in a TNF-α-treated NCM-460 cell colitis model, the apoptotic markers described above were all decreased. In conclusion, our data indicates that ARP3 might promote the apoptosis of IECs in UC, revealing a potential molecular target for treating UC.
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Authors | Shi-Qing Zhang, Wen-Kai Ni, Ming-Bing Xiao, Feng Jiang, Cui-Hua Lu, Rui-Hua Wang, Run-Zhou Ni |
Journal | Pathology, research and practice
(Pathol Res Pract)
Vol. 215
Issue 2
Pg. 235-242
(Feb 2019)
ISSN: 1618-0631 [Electronic] Germany |
PMID | 30396755
(Publication Type: Journal Article)
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Copyright | Copyright © 2018 Elsevier GmbH. All rights reserved. |
Chemical References |
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Topics |
- Actin-Related Protein 3
(metabolism)
- Animals
- Apoptosis
(physiology)
- Cell Line
- Colitis, Ulcerative
(metabolism, pathology)
- Epithelial Cells
(metabolism, pathology)
- Humans
- Intestinal Mucosa
(metabolism, pathology)
- Mice
- Mice, Inbred C57BL
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