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Two-year grant from Pfizer Inc. to UC Riverside will allow exploration of a therapeutic target to correct intestinal barrier defects
By Iqbal Pittalwala on April 7, 2017
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Declan McCole is an associate professor of biomedical sciences in the School of Medicine at UC Riverside. Photo credit: UCR School of Medicine.
RIVERSIDE, Calif. – Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the intestine that includes Crohn’s disease and ulcerative colitis. A protective protein that plays a key role in this disease is “T-cell protein tyrosine phosphatase” or TCPTP.
TCPTP protects the intestinal epithelial barrier function (the body’s intestinal lining has epithelial cells that form a barrier so that bacteria in the gut do not pass on into the rest of the body) and is encoded by a gene associated with not just IBD, but also celiac disease and type 1 diabetes. Some patients with these diseases exhibit loss-of-function mutations in this gene, resulting in loss of TCPTP activity, and have a compromised (or reduced) intestinal epithelial barrier function.
Declan McCole, Ph.D., an associate professor of biomedical sciences in the School of Medicine at the University of California, Riverside, has received a two-year grant of $150,000 from Pfizer Inc. to explore a therapeutic target for correcting intestinal barrier defects in IBD patients who have TCPTP mutations.
“These defects result in increased intestinal permeability – a major contributor to chronic inflammatory diseases of the intestine such as IBD,” McCole said.
He explained that although TCPTP mutations increase the risk of developing IBD, there are no therapeutic strategies aimed at correcting the consequences of these mutations.
The Pfizer Inc. grant will allow his lab to test multiple strategies to restore barrier function in intestinal epithelial cells affected by reduced TCPTP activity. In such cells, the lab plans to interrupt a signaling pathway called “JAK-STAT” that plays a role in increasing intestinal ...
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