Von Willebrand factor delays liver repair after acetaminophen-induced acute liver injury in mice.

ABSTRACT:

Background & aim

Acetaminophen (APAP)-induced acute liver failure is associated with substantial alterations in the hemostatic system. In mice, platelets accumulate in the liver after APAP overdose and appear to promote liver injury. Interestingly, patients with acute liver injury have highly elevated levels of the platelet-adhesive protein von Willebrand factor (VWF), but a mechanistic connection between VWF and progression of liver injury has not been established. We tested the hypothesis that VWF contributes directly to experimental APAP-induced acute liver injury.

Methods

Wild-type mice and VWF-deficient (Vwf^-/-) mice were given a hepatotoxic dose of APAP (300 mg/kg, i.p.) or vehicle (saline). VWF plasma levels were measured by ELISA, and liver necrosis or hep

SUBMITTER: Groeneveld D 

PROVIDER: S-EPMC6941657 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature