Summary
There are clear but poorly understood differences in the etiology and prognosis of thrombotic diseases in men and women. Due to the fact that platelets play a central role in the formation of occlusive thrombi in atherosclerotic coronary arteries, previous studies have examined whether sex differences exist for platelets, and have obtained conflicting results. Additionally, due to the increased use of genetically modified mouse models to explore the molecular mechanisms underlying platelet activation and thrombotic disorders, it is critical to determine if sex is a confounding variable. Our study of the role of sex differences in platelet function was designed to utilise purified platelets from inbred paired female/male littermates in order to minimise genetic and environmental variability. In the current study, we demonstrate that platelet adhesion to and spreading on immobilised fibrinogen, thrombin or collagen was equivalent for both female and male mouse platelets. The ability of the soluble agonist thrombin or convulxin to potentiate platelet Pselectin exposure, fibrinogen binding, or adhesion and spreading on immobilised fibrinogen was equivalent for both female and male mouse platelets. Our data show that an equivalent degree of platelet adhesion and aggregation on collagen or fibrinogen under shear flow was observed for both female and male mouse platelets. In conclusion, our data would argue against an intrinsic difference for female mouse platelets in regulating the major functional platelet responses: platelet adhesion, spreading, or aggregation under flow.
Keywords
Platelet activation - platelet spreading - flow adhesion - sex differences
