Platelet-leukocyte aggregates and derived microparticles in inflammation, vascular remodelling and thrombosis

Abstract

As a result of vascular injury, activated platelets will rapidly interact with circulating platelets, via membrane glycoprotein complex alphaIIbbeta3 (GPIIb-IIIa) and fibrinogen, to form a thrombus or a plug preventing fatal bleeding. In addition, platelets interacting with ruptured atherosclerotic plaques or with the surface of diseased vessels can aggregate and induce ischemia that prevents blood flow. However, increasing evidence has also shown that circulating platelets interact with leukocytes and endothelial cells, via specific adhesion molecules, in inflammation, vascular remodelling and thrombosis. The aim of this chapter is to present the importance of cell-cell interactions involving platelets and leukocytes in events related to inflammation, coagulation, vascular remodelling and thrombosis. A key adhesion molecule implicated in platelet interaction with leukocytes is P-selectin, also known as CD62P. It is present on activated platelets and endothelial cells, and its counterpart on leukocytes is known as P-selectin glycoprotein ligand-1 (PSGL-1). A critical co-factor leading to leukocyte activation in platelet-monocyte aggregate formation is the presence of a chemokine known as RANTES. It acts in concert with platelet P-selectin and PSGL-1 in monocyte stimulation.

The Influence of Hyperlipidemia on Platelet Activity Markers in Patients after Ischemic Stroke

“…Relevant studies have also reported a significantly higher percentage of PDMPs in patients with cerebrovascular events relating to large and small vessels than in healthy subjects [26]. PDMPs play a role in the normal hemostatic response to vascular injury, but on the other hand, it is also possible that the local generation of PDMPs in atherosclerotic arteries may promote arterial occlusion [27]. Thus, persistent elevated blood concentrations of PDMPs may be a marker of the increased risk of ischemic stroke.…”

Association of platelet‐monocyte aggregates with platelet activation, systemic inflammation, and myocardial injury in patients with non‐st elevation acute coronary syndromes

“…2 Inflammation is believed to play a decisive initial and perpetuating role in the thrombotic transformation of this plaque, 3,4 and platelet activation is central to the formation of thrombus. 5 This increased state of inflammation is mainly paralleled by activation of platelets with surface-exposing P-selectin, which tethers the platelet to monocyte via P-selectin glycoprotein ligand-1 (PSGL-1) to form platelet-monocyte aggregates (PMA). The close interaction between monocytes and platelets leads to leukocyte activation and cell-adhesion molecule expression, and activates the release of enzymes such as Matrix Metalloproteinases (MMPs), which degrade the subendothelial basement membrane, leading to subsequent plaque rupture or thrombogenicity.…”

Increased Formation of Monocyte-Platelet Aggregates in Ischemic Heart Failure

“…1 Platelets are the major cellular component of thrombosis, 2 and patients with HF have enhanced platelet activation, as reflected by increased whole blood aggregation, 3 high mean platelet volume, 4 and increased platelet P-selectin surface exposure. 5 In addition to roles in hemostasis and thrombosis, platelets are also able to regulate the activity of other cell types, and cross-talk between monocytes and platelets is reflected by formation of monocyte-platelet aggregates (MPAs).…”