However, work published in recent years shows that the role of platelets is not confined to maintaining vascular integrity and thrombosis as they play an important role in inflammation, cancer dissemination, wound healing and the separation of blood and lymphatic vessels during development. Multiple therapeutic targets have been identified and used in the development of anti-thrombotic drugs. The key role of platelets in haemostasis and thrombosis has been documented for many years ( 6, 7). Haemostasis is a physiological process that maintains the fluidity of the blood and prevents bleeding during vascular injury. They are used as secretion markers in flow cytometry ( 3– 5). During platelet activation, the contents of the granules are secreted and a number of granule-specific proteins are detected on the platelet surface. Platelet cytoplasm contains numerous organelles, in particular some mitochondria, glycogen grains, alpha and dense granules and lysosomes. It also helps to release the contents of the granules.
It plays an important role in platelet biology and, more specifically, in maintaining and changing the shape of platelets during activation and aggregation. The plasma membrane is supported by a highly developed cytoskeleton, consisting of microtubules and actin microfilaments ( 1). This system serves mainly as a membrane reservoir as the platelets change shape ( 1, 2). It contributes to the uptake of external elements into the platelets and to the release of granule contents upon activation. The OCS corresponds to deep invaginations of the plasma membrane and runs continuously along the cell surface. The study of platelet morphology by electron microscopy has highlighted three major components: i) the plasma membrane with an open canalicular system (OCS), ii) the cytoskeleton and iii) the various intracellular organelles ( 1). They then spread and aggregate, forming a platelet plug to stop bleeding from capillaries and small vessels ( 1). They lose their discoid shape and become spherical, emitting long filopodia to facilitate their adhesion. Following injury to the vascular wall, they interact very quickly with the subendothelium and are activated to prevent bleeding. These small, disc-shaped cells circulate at a rate of 150,000 to 350,000 platelets per μl of blood. As a general rule, all of the studies presented in this review show that platelets are capable of covering most of the stages of inflammation, primarily through the CD40L/CD40 interaction, thus confirming their own role in this pathophysiological condition.īlood platelets are anucleate cells produced by the fragmentation of megakaryocytes (MK). Platelets are involved in the direct activation of immune cells, polynuclear neutrophils (PNNs) and dendritic cells via the CD40L/CD40 complex. Platelet activation also contributes to the extensive release of anti- or pro-inflammatory mediators such as IL-1β, RANTES (Regulated on Activation, Normal T Expressed and Secreted) or CD154, also known as the CD40-ligand. Platelets also have a major inflammatory and immune function in antibacterial defence, essentially through their Toll-like Receptors (TLRs) and Sialic acid-binding immunoglobulin-type lectin (SIGLEC). Activated platelets can also secrete the contents of their granules, notably the growth factors contained in the α-granules, which are involved in platelet aggregation and maintain endothelial activation, but also contribute to vascular repair and angiogenesis. Activated platelets adhere to the damaged endothelium by means of glycoproteins on their surface, forming the platelet plug. Platelets are anucleate cytoplasmic fragments derived from the fragmentation of medullary megakaryocytes.