Platelet PMDs in hemostasis and thrombosis. (A) Thrombosis occurs at sites of breached endothelium, leading to exposure of subendothelial collagen, platelet GPVI activation, platelet hemostatic plug formation, membrane ballooning, microvesiculation, and PS exposure (top). (B) Thrombus formation may also occur intravascularly because of platelet-matrix protein interaction, a process more likely to occur in venous beds, leading to deep vein thrombosis.14,15 Here, soluble and/or diffusible platelet agonists may activate platelets and lead to thrombosis intravascularly without substantial vessel injury. In panels A-B, thrombin may feed back on the platelets to further potentiate PS exposure, leading to further thrombin generation. (C) A stable hemostatic plug is formed after injury, which markedly exposes the subendothelial matrix. In addition to activated and ballooned platelets, support for hemostasis is provided via the release or generation of tissue factors and by nonplatelet sources of PS; namely, red blood cells,16-19 macrophages,20,21 neutrophils,22 monocytes,21,23 and cells of the vessel intima layer,24-27 which are also able to expose PS and present catalytic surfaces for localized thrombin generation.
