Human Platelet Biology

A brief scientific summary of human platelets. Discussed is platelet biology, the physiological role following activation and finally, the structure of these cells.

Platelet Biology

The first step of coagulation requires specialized cells referred to as platelets.  These cells circulate freely in the blood.  Following blood vessel damage, platelets become activated when subendothelial and blood factors interact.  The activated platelets then adhere to both the exposed subendothelial surface and each other forming a plug at the site of vascular damage.  If inactivate, platelets do not adhere to either the inside of blood vessels or to each other.

 

Platelet Physiology

The role of platelets in coagulation has been extensively studied since the first description of platelets by Max Schultze.  Platelet response is a closely integrated three phase process starting with adhesion, followed by activation leading to shape change and secretion with aggregation.  However, these three stages are not clearly separated and all three involve platelet activation.  Adhesion is the binding and localization of platelets to the damaged vessel region, while aggregation is the accumulation of platelets into the formation of a haemostatic plug.  Platelets become stimulated by soluble agents (ADP, thrombin or thromboxane A2) or by interactions with adhesion molecules (collagen or vWF).  Soluble agents secreted from platelets at the site of injury in turn, activate and recruit additional platelets.  Although activated platelets initiate coagulation in many ways, one mechanism involves phosphatidylserine, which is typically expressed on the cytoplasmic side of the platelet membrane.  The reorientation of phosphatidylserine to the extracellular side of the membrane activates Factor Xa and Va, which in turn catalyze the generation of thrombin from prothrombin.

Platelet Structure

Platelets originate in the bone marrow from megakaryocytes and are discoid anuclear cells.  Moreover, platelets are the smallest cells in the blood.  On the surface of the platelet are small pits, which serve as openings of the open canalicular system (OCS).  The OCS, formed via extensive invagination of the plasma membrane, is an intricate tunneling system through which platelet granules extrude their constituents.  Surrounding platelets is a plasma membrane phospholipid bilayer with embedded phosphatidylserine and phosphoinositide residues on the cytoplasmic side.   In contrast, on the extracellular side of the membrane, are many transmembrane receptors, which function as receptors for stimulatory or inhibitory stimuli.  These include glycoproteins for adhesive molecules, G-protein coupled receptors for activation or inhibition and platelet endothelial cell adhesion molecule-1 for leukocyte binding.  The cytoplasmic tails of these receptors are proximal to the intraplatelet contractile system which includes actin-binding proteins and actin filaments.  Within platelets is an elaborate cytoskeleton which consists primarily of actin filaments, but also includes a submembranous microtubule coil.  Actin and myosin play roles in the shape change of platelets following stimulation and in the centralization of granules for secretion.  A microtubule coil beneath the plasma membrane, composed of tubulin, helps to maintain the discoid shape of platelets.

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