Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2
2018
Abstract Introduction Recent genome wide association studies (GWAS) identified a novel susceptibility locus for thrombosis, harbouring the SLC44A2 gene which encodes the
Solute Carrier Family44 Member 2 protein (SLC44A2). Thus far, SLC44A2 has not been studied in the context of thrombosis, and may be a unique contributor to thrombotic disease. Here we utilize mice lacking SLC44A2 ( Slc44a2 −/− ) to evaluate a possible role of SLC44A2 in
hemostasis. Methods Slc44a2 −/− mice were evaluated in key aspects of normal
hemostasisincluding a challenge of vascular damage by applying laser induced injury to the
cremaster muscle
arteriole. Results Slc44a2 −/− mice had comparable levels of thrombin generation and gene expression of coagulation related genes, as compared to littermate wild type controls. Lower levels of circulating plasma
Von Willebrand factor(VWF) were measured in Slc44a2 −/− mice, while no difference in VWF multimerization or vascular localization was detected. Upon in vivo laser injury of the cremaster
arterioles, we detected an impairment of
clot formationfor Slc44a2 −/− mice. Conclusions Although mice lacking SLC44A2 are normal for several
hemostasisparameters, we do observe a reduction of plasma VWF levels and an altered response upon vascular damage, which suggests that SLC44A2 contributes to
hemostasisupon injury. These findings are in line with the reported GWAS data and support further research on SLC44A2 in thrombosis.
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