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Updated: Mar 24, 2026
Stenosis of the Inferior Vena Cava: A Murine Model of Deep Vein Thrombosis
Published on: December 22, 2017
GPVI deficiency reduces clot size and murine thrombosis in normoglycaemic but not hyperglycemic conditions
Julia S Gauer1, Cédric Duval1, Helen R McPherson1
1Discovery and Translational Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Background:
Glycoprotein (GP)VI is involved in platelet activation, procoagulant phenotype development and reactive oxygen species (ROS) production. Patients with diabetes have altered platelet reactivity and abnormal clot structure, contributing to elevated thrombosis risk. The role of GPVI in clot formation in hyperglycemia is under-investigated.
Objectives:
To compare the effect of GPVI-deficiency on ROS production and ex vivo and in vivo clot formation in normo- vs hyperglycemic mice.
Methods:
Wild-type (WT) and GPVI-deficient (GPVI-/-) mice had access to hyperglycemic (30% sucrose) or normoglycaemic (standard) diet for 8-weeks. ROS and mitochondrial activity (CS) were measured in isolated platelets. Clot contraction was performed with whole blood. Thrombus formation in vivo was assessed by inferior vena cava (IVC) ligation.
Results:
Hyperglycemia increased ROS and CS activity in WT but not GPVI-/- mice. Clot weight was decreased in GPVI-/- vs WT mice in normoglycaemia, but these effects were lost in hyperglycemia. Clot weight after IVC ligation was reduced in GPVI-/- vs WT mice in normoglycaemia, with the inverse observed in hyperglycemia.
Conclusions:
Our data suggest that clot formation is affected differentially by absence of GPVI in normo- vs hyperglycemia, supporting a role for GPVI in thrombosis under normoglycaemic conditions only.
