Figure 6
From: Disruption of the kringle 1 domain of prothrombin leads to late onset mortality in zebrafish
Loss of thrombin activity results in defects in secondary hemostasis. (A) Larvae were immobilized in agarose, subjected to laser-mediated endothelial injury (green arrow) of the venous (PCV, blue) or arterial (dorsal aorta, red) circulation, and followed for 2 minutes by a blinded observer. (B) Genetic ablation of f2 resulted in the inability to form induced PCV thrombi at 3 dpf and was not influenced by inhibiting fibrinolysis (ɛ-aminocaproic acid treatment, blue). (C) Overexpression of human F2 cDNA (blue) rescued the ability to form thrombi in the PCV at 3 dpf. (D) Homozygous mutant larvae demonstrated a significant impairment in arterial thrombus formation at 5 and 6 dpf without any changes in the time to initial thrombocyte attachment (E). (F) The number of thrombocytes attached to the site of injury in 2 minutes was significantly increased at 6 dpf in f2 homozygous mutants. Statistical significance assessed by Mann-Whitney U testing.
