Definitions of platelets often describe them as ‘fragments’ of cells and in figures they are often small blobs with little indication of what they actually do. At the turn of the 20th century they were even dismissed as ‘the dust of the blood’. This implication that platelets are passive bits of cytoplasm floating through the blood is immensely misleading. Like erythrocytes they lack a nucleus and superficially at least also appear to barely meet the definition of a cell. However, there are a number of major differences which have important implications for the origin and treatment of blood disorders.
|ER, mitochondria, endosomes, lysosomes.||Organelles||None|
|Highly organised microfilaments.|
Cortical microtubule ring.
|Cytoskeleton||Highly organised microfilaments.|
|Wrinkled, invaginated discoid|
to highly extruded.
|Form||Smooth, flexible, discoid.|
|Clotting, inflammatory signalling, protein secretion, wound repair.||Function||Oxygen transport, pH balance.|
The 3 ‘A’s of haemostasis
A key role of platelets is haemostasis; they constantly plug microscopic sites of injury in blood vessels. If this does not occur correctly and promptly, it results in bleeding disorders of varying severity. On the other hand, there are times when the platelet clotting response is undesirable or excessive and this is the target of anti-platelet drugs to minimise the risk of thrombosis and embolism.
Platelets carry cell surface receptors which recognise proteins such as collagen and von Willebrand Factor that get exposed by tissue damage. When the receptors bind to these receptors, it makes the platelets adhere to the site.
Adhesion receptors trigger intracellular signalling pathways that activate the platelet causing it to radically change shape and release secretory granules. Activation can also occur in response to inflammatory signals, including those released by other platelets.
A major component of the granules released by activated platelets is sticky adhesion proteins which, together with other signals triggered by activation, make platelets clump together in aggregates to seal off the damage.
It should be stressed that this model of activation and aggregation is a major simplification. The steps do not happen in isolation and an individual platelet might be activated by tissue damage or by factors secreted by other platelets. An adherent platelet may also be activated and aggregating. In particular, signals other than collagen and von Willebrand Factor are gaining increasing attention as critical factors in the body’s response to infection or trauma and as potential therapeutic targets.