Do cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner?
Both cocaine and metabolites benzoylecgonine and cocaethylene induced endothelial VWF secretion, possibly explaining thrombotic risk after cocaine ingestion. VWF secretion is likely to vary between vascular beds, with brain endothelial cells being particularly sensitive. These results suggest that clinical management of cocaine-induced ischemia may benefit from therapies aimed at disrupting the VWF-platelet interaction.
PAI-2 promotes adipose tissue development in mice via a mechanism independent of its antifibrinolytic effect.