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Factor XIII Deficiency Does Not Prevent FeCl3-induced Carotid Artery Thrombus Formation in Mice

Background: The compositions of venous (red blood cell-rich) and arterial (platelet-rich) thrombi are mediated by distinct pathophysiologic processes; however, fibrin is a major structural component of both. The transglutaminase factor XIII (FXIII) stabilizes fibrin against mechanical and biochemical disruption and promotes red blood cell retention in contracted venous thrombi. Previous studies have shown FXIII inhibition decreases whole blood clot mass and therefore, may be a therapeutic target for reducing venous thrombosis. The role of FXIII in arterial thrombogenesis is less studied, and the particular contribution of platelet FXIII remains unresolved. Objective: To determine whether FXIII reduction prevents experimental arterial thrombogenesis. Methods: Using wild‐type mice and mice with genetically imposed deficiency in FXIII, we measured thrombus formation and stability following ferric chloride–induced arterial thrombosis. We also determined the impact of FXIII on the mass of contracted platelet‐rich plasma clots. Results: Following vessel injury, F13a+/+ , F13a+/− , and F13a−/− mice developed occlusive arterial thrombi. FXIII deficiency did not significantly reduce the incidence or prolong the time to occlusion. FXIII deficiency also did not alter the timing of reflow events or decrease platelet‐rich clot mass. Conclusions: FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.