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Platelet Plug Formation
Injury
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Damage to endothelial cells and exposure of collagen
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Von Willebrand Factor (vWF) is released by damaged endothelial cells
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vWF binds to exposed collagen.
Platelet Adhesion
Through following receptors, the platelet attaches to the exposed collagen:
Gp Ib ↔ vWF ↔ Collagen
Gp Ia/IIa ↔ Collagen
Gp VI ↔ Collagen
Platelet Activation & Release Reaction
Activation of the receptors → intracellular signaling events → release of alpha and dense granule.
Alpha (α) granules:
Growth factors → Wound healing
Von Willebrand factor → Platelet aggregation
Fibrinogen → Platelet aggregation and coagulation
Factor V → Coagulation
Dense granules:
ADP → Platelet aggregation
Serotonin → Vasoconstriction
Calcium → Coagulation
Enxyme COX-1 and thromboxane synthase synthesize TxA2 from membrane phospholipids → TxA2 is released into the blood.
Parallel coagulation cascade on platelet surface → formation of thrombin → released into the blood.
Platelet changes shape (extend finger-like projection) → Increase surface area.
Conformational changes in Gp IIb/IIIa → binds with fibrinogen.
Platelet Aggregation
More platelets are activated by:
ADP ↔ P2Y12
TxA2 ↔ TP
Thrombin ↔ PAR-1 (Protease-activated receptor-1)
Activated platelets undergo similar changes as described above including:
Conformational changes in Gp IIb/IIIa → bind with fibrinogen which acts as bridge between two platelets. vWF can also serve as bridge between platelets.
More release reaction→ More platelet activation → So on… → in this way, platelets are recruited till the wound is plugged → this plug is called primary hemostatic plug or primary platelet plug → fibrin synthesized by coagulation strengthens it → called secondary plug.