PUBLICATION
Ace Deficiency Induces Intestinal Inflammation in Zebrafish
- Authors
- Wei, M., Yu, Q., Li, E., Zhao, Y., Sun, C., Li, H., Liu, Z., Ji, G.
- ID
- ZDB-PUB-240620-11
- Date
- 2024
- Source
- International Journal of Molecular Sciences 25(11): (Journal)
- Registered Authors
- Li, Hongyan, Liu, Zhenhui
- Keywords
- angiotensin-converting enzyme, enteritis, inflammatory bowel disease, teleost
- MeSH Terms
-
- Animals
- Dextran Sulfate
- Disease Models, Animal
- Inflammation/genetics
- Inflammation/metabolism
- Inflammation/pathology
- Inflammatory Bowel Diseases/genetics
- Inflammatory Bowel Diseases/metabolism
- Inflammatory Bowel Diseases/pathology
- Interleukin-1beta/genetics
- Interleukin-1beta/metabolism
- Intestinal Mucosa/metabolism
- Intestinal Mucosa/pathology
- Intestines/pathology
- Peptidyl-Dipeptidase A*/genetics
- Peptidyl-Dipeptidase A*/metabolism
- Zebrafish*/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 38891786 Full text @ Int. J. Mol. Sci.
Citation
Wei, M., Yu, Q., Li, E., Zhao, Y., Sun, C., Li, H., Liu, Z., Ji, G. (2024) Ace Deficiency Induces Intestinal Inflammation in Zebrafish. International Journal of Molecular Sciences. 25(11):.
Abstract
Inflammatory bowel disease (IBD) is a nonspecific chronic inflammatory disease resulting from an immune disorder in the intestine that is prone to relapse and incurable. The understanding of the pathogenesis of IBD remains unclear. In this study, we found that ace (angiotensin-converting enzyme), expressed abundantly in the intestine, plays an important role in IBD. The deletion of ace in zebrafish caused intestinal inflammation with increased expression of the inflammatory marker genes interleukin 1 beta (il1b), matrix metallopeptidase 9 (mmp9), myeloid-specific peroxidase (mpx), leukocyte cell-derived chemotaxin-2-like (lect2l), and chemokine (C-X-C motif) ligand 8b (cxcl8b). Moreover, the secretion of mucus in the ace-/- mutants was significantly higher than that in the wild-type zebrafish, validating the phenotype of intestinal inflammation. This was further confirmed by the IBD model constructed using dextran sodium sulfate (DSS), in which the mutant zebrafish had a higher susceptibility to enteritis. Our study reveals the role of ace in intestinal homeostasis, providing a new target for potential therapeutic interventions.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping