Key result
Activated protein C inhibits thrombin-activated bovine platelet prothrombin-converting activity in a time-dependent manner, causing a parallel loss of factor Xa receptor sites.
Why the study?
Does activated protein C inhibit platelet prothrombin-converting activity in thrombin-activated bovine platelets?
Does activated protein C inhibit platelet prothrombin-converting activity in thrombin-activated bovine platelets?
Activated protein C inhibits platelet prothrombin-converting activity by causing a loss of factor Xa receptor sites, suggesting a role in clotting regulation.
Bovine platelet findings require human validation before any clinical consideration; leaves open APC's role in regulating human coagulation.
Bovine platelets that have been activated by thrombin facilitate the conversion of prothrombin to thrombin in the presence of calcium ions and factor Xa. Activated protein C, a vitamin-K-dependent plasma protein, inhibits this platelet prothrombin-converting activity. The inhibition is time dependent and is not reversed by increasing concentrations of factor Xa. However, factor Xa is able to protect the platelet prothrombin-converting activity from inactivation by activated protein C. The activated protein C causes a parallel loss of factor Xa receptor sites and platelet prothrombin-converting activity. Activated protein C may contribute to the regulation of clotting through inactivation of the platelet prothrombin-converting activity.
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Comp et al. (1979) studied this question. Activated protein C was evaluated on Platelet prothrombin-converting activity. Activated protein C inhibits thrombin-activated bovine platelet prothrombin-converting activity in a time-dependent manner, causing a parallel loss of factor Xa receptor sites.
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