Abstract
Procoagulant platelets are a subtype of activated platelets that sustains thrombin generation in order to consolidate the clot and stop bleeding. This aspect of platelet activation is gaining more and more recognition and interest. In fact, next to aggregating platelets, procoagulant platelets are key regulators of thrombus formation. Imbalance of both subpopulations can lead to undesired thrombotic or bleeding events. COAT platelets derive from a common pro-aggregatory phenotype in cells capable of accumulating enough cytosolic calcium to trigger specific pathways that mediate the loss of their aggregating properties and the development of new adhesive and procoagulant characteristics. Complex cascades of signaling events are involved and this may explain why an inter-individual variability exists in procoagulant potential. Nowadays, we know the key agonists and mediators underlying the generation of a procoagulant platelet response. However, we still lack insight into the actual mechanisms controlling this dichotomous pattern (i.e., procoagulant versus aggregating phenotype). In this review, we describe the phenotypic characteristics of procoagulant COAT platelets, we detail the current knowledge on the mechanisms of the procoagulant response, and discuss possible drivers of this dichotomous diversification, in particular addressing the impact of the platelet environment during in vivo thrombus formation.
Highlights
Published: 25 February 2022Procoagulant platelets are a subpopulation of platelets appearing upon strong activation, which localize and enhance thrombin generation at sites of vascular injury by expressing negatively charged phospholipids and sustaining the formation of the tenase and prothrombinase complexes on their surface [1]
Procoagulant platelets promote the deposition of fibrin in order to stabilize and limit the primary platelet plug, which is composed of aggregating platelets, the main platelet subpopulation [2]
Several families of Cl- channels are found in platelets, such as chloride channel proteins (CLCN), chloride intracellular channels (CLIC), and calcium-activated chloride channels (CaCC) within the TMEM16 family [121]
Summary
Procoagulant platelets are a subpopulation of platelets appearing upon strong activation, which localize and enhance thrombin generation at sites of vascular injury by expressing negatively charged phospholipids and sustaining the formation of the tenase and prothrombinase complexes on their surface [1]. This balance seems to be altered in bleeding diatheses [6,7] and hemorrhagic strokes [8,9]. Initial thrombin is produced due to TF expresplatelets at the site of injury. Initial thrombin is produced due to TF expresand shape change: Platelets bind to collagen receptor GPIa-IIa. Even though GPIb-IX-V and GPIasion. Platelet GPIb-IX-V complex interacts with the VWF deposited on collagen
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