Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2

Julia Tilburg, Reheman Adili, Thankam S. Nair, Megan E. Hawley, David C. Tuk, Madeline Jackson, Henri M. Spronk, Henri H. Versteeg, Thomas E. Carey, Bart J. M. van Vlijmen, Chrissta X. Maracle*, Michael Holinstat

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Introduction: Recent genome wide association studies (GWAS) identified a novel susceptibility locus for thrombosis, harbouring the SLC44A2 gene which encodes the Solute Carrier Family 44 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 hemostasis including 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 formation for Slc44a2(-/-) mice.

Conclusions: Although mice lacking SLC44A2 are normal for several hemostasis parameters, we do observe a reduction of plasma VWF levels and an altered response upon vascular damage, which suggests that SLC44A2 contributes to hemostasis upon injury. These findings are in line with the reported GWAS data and support further research on SLC44A2 in thrombosis.

Original languageEnglish
Pages (from-to)155-159
Number of pages5
JournalThrombosis Research
Publication statusPublished - Nov 2018


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