SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis.

ABSTRACT:

Background

Genome wide association studies (GWAS) identified SLC44A2 as a novel susceptibility gene for venous thrombosis (VT) and previous work established that SLC44A2 contributed to clot formation upon vascular injury.

Objective

To further investigate the role of SLC44A2 in VT by utilizing SLC44A2 deficient mice (Slc44a2^-/- ) in two representative disease models.

Methods

Mice were included in a hypercoagulability model driven by siRNA-mediated hepatic gene silencing of anticoagulants Serpinc1 (antithrombin) and Proc (protein C) and a flow restriction (stenosis) model induced by partial ligation of the inferior vena cava.

Results

In the hypercoagulability model, no effect in onset was observed in Slc44a2^-/

SUBMITTER: Tilburg J 

PROVIDER: S-EPMC7383581 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature