Platelet Glycoprotein analysis

Platelets are anucleate fragments of the cytoplasm of their parent cell, the megakaryocyte. They circulate predominantly at the margins of blood vessels in a dormant, resting state, but are capable of a rapid and dramatic response to various stimuli arising from vessel trauma. They have a complex structure that facilitates their specialised functions, of which the main ones are listed below:
● Interaction with collagen-captured VWF to form the initial barrier to blood loss
● Propagate the clot via platelet aggregation
● Provide the platform for secondary haemostasis
● Localisation mechanisms
● Maintain endothelial junction integrity.
Exposure of sub-endothelial collagen after vessel trauma promotes binding of VWF which tethers platelets via their GpIb receptor. Blood flow rolls the platelet over where it forms stable associations via separate collagen binding receptors which also serves to activate the platelet. Activated platelets change their shape to promote effective physical interaction and release of the contents of cytoplasmic granules which activate more platelets and promote platelet-to-platelet aggregation via fibrinogen bridging of receptors on adjacent platelets. Biochemical pathways are also activated to promote aggregation, and the phospholipid membrane re-organises to promote localisation of secondary haemostasis to stabilise the platelet plug. Reduced platelet numbers, receptor deficiency/dysfunction, granule deficiency or granule content deficiency, biochemical abnormalilties and drug interactions can lead to bleeding disorders. Quantitative receptor deficiencies can be detected using labelled antibodies in flow cytometry.