ADAMTS13 Deficiency Worsens Colitis and Exogenous ADAMTS13 Administration Decreases Colitis Severity in Mice.

ABSTRACT:

Background

Inflammatory bowel disease (IBD) affects 1.6 million people in the United States. IBD is associated with an increased risk of thrombosis, which rises with disease activity. The pathogenesis of IBD and its increased thrombotic risk is not completely understood. Ultra large von Willebrand factor (ULVWF) multimers are secreted from activated endothelium, leading to recruitment of platelets and leukocytes. A disintegrin and metalloproteinase with thrombospondin type I repeats motif 13 (ADAMTS13) cleaves highly adhesive ULVWF into smaller, less bioactive, multimers, releasing them into circulation. Mice deficient in ADAMTS13 (ADAMTS13^-/-) have heightened inflammatory and thrombotic responses.

Objectives

We hypothesized that upon colitis induction, ADAMTS13

SUBMITTER: Zitomersky NL 

PROVIDER: S-EPMC5782810 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature