Introduction

As a consequence of vessel wall damage, circulating platelets adhere to subendothelial ligands, targeting them to the site of injury. Adhering platelets undergo a multitude of signalling events, which result in platelet activation and spreading. Whereas platelet spreading on collagen and binding of adhesive proteins facilitate subsequent recruitment of additional platelets from the circulation, the activation of platelets also leads to the controlled release of their contents. Thus, the local secretion of further agonists of platelet activation, via a signalling controlled exocytosis reaction, contributes to the rapid recruitment of circulating platelets to the injury site; secreted proteins also facilitate fibrin formation.

In a forming platelet aggregate, as a result of inside-out signalling, the platelet receptor for fibrinogen, i.e. GPIIb/IIIa, is assembled. The binding of fibrinogen to this receptor not only enables platelet cross-linking, but further contributes to the ongoing platelet activation via outside–in signaling. This highly localized enhancement of ongoing platelet activation leads to marked degranulation in a confined area. Thus, platelet aggregate formation occurs as the result of both platelet adhesion and localized secretion, leading to the formation of a platelet plug, in which large numbers of platelets are completely degranulated.

Platelet granules and exocytosis

Morphologically, three types of platelet granules can be released: dense core granules (δ-granules), α-granules and platelet lysosomes (λ-granules).