Platelet aggregation
Platelet aggregation is a crucial step in the formation of a blood clot. It occurs when platelets (small blood cells) clump together at the site of a blood vessel injury to form a temporary plug, which helps stop bleeding. This process is part of primary hemostasis, which precedes the coagulation cascade.
Steps of Platelet Aggregation:
-
Vessel Injury and Platelet Activation:
- When a blood vessel is damaged, the endothelial cells lining the vessel become disrupted.
- Collagen and von Willebrand factor (vWF), exposed in the subendothelial layer, interact with platelets.
- Platelets adhere to the exposed collagen through specific receptors, such as glycoprotein Ib (GPIb).
-
Platelet Shape Change and Degranulation:
- Platelets change shape from disc-like to more spherical with projections to increase surface area.
- Activated platelets release stored granules containing ADP, thromboxane A2 (TXA2), and serotonin, which promote further platelet activation and aggregation.
-
Recruitment of Additional Platelets:
- The released ADP and TXA2 activate nearby platelets, causing them to express Glycoprotein IIb/IIIa (GPIIb/IIIa) receptors.
- These receptors are key in cross-linking platelets to form aggregates.
-
Fibrinogen Binding and Aggregation:
- Fibrinogen, a plasma protein, binds to the GPIIb/IIIa receptors on adjacent platelets, acting as a bridge that links platelets together.
- This cross-linking leads to the formation of a platelet plug.
-
Stabilization of the Platelet Plug:
- The platelet plug is initially unstable and requires reinforcement by the fibrin network, formed during the coagulation cascade.
- Fibrin strands weave through the aggregated platelets, stabilizing the clot.
Key Players in Platelet Aggregation:
- ADP and TXA2: Promote platelet activation and aggregation.
- GPIIb/IIIa receptors: Allow platelets to bind fibrinogen and aggregate.
- Fibrinogen: Bridges platelets by binding to GPIIb/IIIa.
- Von Willebrand Factor (vWF): Helps platelets adhere to the vessel wall by binding to both collagen and GPIb on platelets.
Platelet aggregation is regulated by factors that prevent excessive clotting, such as prostacyclin (PGI2) and nitric oxide (NO), which are released by healthy endothelial cells and inhibit platelet activation.