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Picture: Declan McCole is a professor of biomedicine at the University of California, Riverside
.
A research team led by biomedical scientists at the University of California, Riverside, has identified a novel mechanism to lose the mutant gene PTPN2, which has been found in many patients with inflammatory bowel disease, or inflammatory bowel disease, that affects the maintenance of intestinal epithelial cells.
.
The intestinal epithelium is a layer of cells that plays an important role in human health.
It provides a barrier while also allowing the absorption of nutrients and water
.
Intestinal epithelial cells are necessary for regulating immune function, communicating with the intestinal microbiota, and protecting the intestine from pathogen infection, all of which rely heavily on a complete epithelial barrier
IBD is a chronic intestinal disease.
Inflammation and leakage of the intestinal lining affects approximately 3 million Americans
.
Increased intestinal leakage has recently been shown to increase the risk of IBD
"This new publication is a culmination of body work in my laboratory to identify how loss of mutations in PTPN2 can increase intestinal permeability or leakage," said Declan McCole, Professor of Biomedical Sciences at the University of California School of Medicine , Led this research to be published in the "Journal of Clinical Research"
.
The journal selected this research paper as the "editor's highlight
In this study, which was carried out on mice, human cells and tissues of patients with inflammatory bowel disease, McCole and his colleagues found that patients with IBD carry the loss of function PTPN2 mutation, claudin-2 expression, one This kind of protein, which causes the loss of water and sodium to enter the intestines, promotes diarrhea, is increased
.
Through the mouse model, McCole's laboratory discovered a dual mechanism that explained the increased expression of claudin-2 and the cause of fluid loss
McCole explained that PTPN2 usually inhibits the expression of claudin-2
.
The loss of PTPN2 function that occurs in IBD eliminates this brake and allows increased fluid loss
"In addition, PTPN2 also promotes an endogenous factor called matripase, which removes cldin-2 from the cell membrane area, where it regulates its effects and allows fluid loss," McCole said
.
The cumulative effect of reduced PTPN2 activity on the two mechanisms is an increase in fluid loss
.
The researchers demonstrated that this defect can be reversed by treating cells lacking PTPN2 with recombinant- or synthetic-matrix enzymes
McCole said: "Our work has improved the understanding of how the IBD gene affects the physiological changes in patients, leading to their symptoms
.
" "This also supports our related work to determine how a class of drugs called JAK inhibitors is used.
The study also showed that a rare PTPN2 mutation recently discovered can cause intestinal epithelial damage in children and increase intestinal epithelial leakage, but it will not cause epithelial cell death
"This suggests that patients with this disease may show'gut leakage' before the full outbreak of the disease," McCole said
Original title:
T-Cell Protein Tyrosine Phosphatase Protects Intestinal Barrier Function by Restricting Epithelial Tight Junction Remodeling
