Which protein released from endothelial cells and platelets leads to increased platelet adhesion?

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Multiple Choice

Which protein released from endothelial cells and platelets leads to increased platelet adhesion?

Explanation:
Endothelial injury exposes subendothelial collagen, and the first step in forming a hemostatic plug is platelet adhesion mediated by von Willebrand factor. Released from endothelial cells and platelets, VWF binds exposed collagen and also attaches to the platelet GPIb receptor, effectively linking the platelets to the damaged site and promoting adhesion. This bridging role is what increases platelet sticking at the injury. Fibrinogen, in contrast, helps platelets stick together to form aggregates by bridging GPIIb/IIIa, not initial adhesion to the vessel wall. Thromboxane A2 drives platelet activation and aggregation and also causes vasoconstriction, not adhesion to collagen. Platelet-derived growth factor is more involved in wound healing and smooth muscle repair than in promoting platelet adhesion.

Endothelial injury exposes subendothelial collagen, and the first step in forming a hemostatic plug is platelet adhesion mediated by von Willebrand factor. Released from endothelial cells and platelets, VWF binds exposed collagen and also attaches to the platelet GPIb receptor, effectively linking the platelets to the damaged site and promoting adhesion. This bridging role is what increases platelet sticking at the injury.

Fibrinogen, in contrast, helps platelets stick together to form aggregates by bridging GPIIb/IIIa, not initial adhesion to the vessel wall. Thromboxane A2 drives platelet activation and aggregation and also causes vasoconstriction, not adhesion to collagen. Platelet-derived growth factor is more involved in wound healing and smooth muscle repair than in promoting platelet adhesion.

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