At the site of atherosclerotic plaque rupture, a gradient of agonist is released, and platelets are recruited to form an initial plug. PGE2 is produced by macrophages in the plaque as well as by activated platelets. The inhibitory phenotype is accompanied by a increased threshold for platelet aggregation, preventing platelet hyperreactivity. In contrast, the potentiating phenotype is associated with a decreased threshold for platelet aggregation, promoting formation of an occlusive thrombus.