Summary
Vascular injury leads to formation of a structured thrombus as a consequence of platelet
activation and aggregation, thrombin and fibrin formation, and trapping of leukocytes
and red cells. This review summarises current evidence for heterogeneity of platelet
responses and functions in the thrombus-forming process. Environmental factors contribute
to response heterogeneity, as the platelets in a thrombus adhere to different substrates,
and sense specific (ant)agonists and rheological conditions. Contraction of platelets
and interaction with fibrin and other blood cells cause further response variation.
On the other hand, response heterogeneity can also be due to intrinsic differences
between platelets in age and in receptor and signalling proteins. As a result, at
least three subpopulations of platelets are formed in a thrombus: aggregating platelets
with (reversible) integrin activation, procoagulant (coated) platelets exposing phosphatidylserine
and binding coagulation factors, and contracting platelets with cell-cell contacts.
This recognition of thrombus heterogeneity has implications for the use and development
of antiplatelet medication.
Keywords
Aggregation - coagulation - heterogeneity - platelets - thrombus formation