Plateletspecific

Platelets are small, colorless cell fragments found in the blood of all vertebrates, playing a crucial role in hemostasis—the process of stopping bleeding. Platelets, also known as thrombocytes, are derived from megakaryocytes, large bone marrow cells that fragment into multiple platelets. These fragments circulate in the bloodstream for about 7–10 days before being removed by the spleen or liver.

Platelets are anuclear, meaning they lack a nucleus, and contain dense granules, alpha granules, and lysosomes that store various proteins and signaling molecules. Their primary function is to form clots by adhering to damaged blood vessel walls and aggregating to form a platelet plug. This process is initiated by exposure to collagen or other subendothelial components when a blood vessel is injured. Platelets release chemicals like adenosine diphosphate (ADP), serotonin, and thromboxane A2, which further promote aggregation and vasoconstriction.

Platelet-specific receptors, such as glycoprotein IIb/IIIa (GPIIb/IIIa) and glycoprotein Ib-IX-V (GPIb-IX-V), are essential for their adhesive and aggregatory functions. GPIIb/IIIa binds fibrinogen, bridging platelets together, while GPIb-IX-V facilitates initial adhesion to von Willebrand factor on damaged vessels. Platelet activation is also regulated by signaling pathways involving calcium ions, phospholipids, and enzymes like phospholipase A2 and cyclooxygenase.

Disorders involving platelet dysfunction, such as thrombocytopenia (low platelet count) or qualitative defects (e.g., Glanzmann’s thrombasthenia or Bernard-Soulier syndrome), can lead to bleeding disorders. Conversely, excessive platelet activation contributes to thrombotic diseases, including deep vein thrombosis and arterial thrombosis. Medications like antiplatelet drugs (e.g., aspirin, clopidogrel) and anticoagulants are commonly used to modulate platelet activity in clinical settings.