A recombinant fragment of von Willebrand factor reduces fibrin-rich microthrombi formation in mice with endotoxemia.

ABSTRACT:

Introduction

Disseminated fibrin deposition in the microvasculature such as in disseminated intravascular coagulation (DIC) arises from uninhibited activated coagulation secondary to sustained systemic inflammation. Currently there is no treatment for DIC. Treating the underlying trigger and supportive care are the current recommendations to manage DIC. This study aims at using recombinant von Willebrand factor (VWF) A2 domain polypeptide to inhibit VWF-mediated platelet adhesion to fibrin and prevent DIC.

Materials and methods

We use flow chamber assay to test the capacity of purified A2 protein to inhibit platelet adhesion to immobilized fibrin(ogen) and platelet-fibrin clot formation. We use a murine model of lipopolysaccharide-induced DIC to examine the effect of A2 prot

SUBMITTER: Nguyen TC 

PROVIDER: S-EPMC5270629 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature