Immune and endothelial cell receptors engaged by platelet-derived extracellular vesicles (PEV receptors)

Platelet-derived extracellular vesicles (PEVs) are small, membrane-enclosed particles released upon platelet activation that function as potent biological effectors in the vascular environment (Varon & Shai, 2015). These vesicles express a variety of surface molecules, such as P-selectin (CD62P) and integrins like GPIIb/IIIa, which allow them to engage specific receptors on immune cells and endothelial cells (Brisson et al., 2017). On immune cells, PEVs primarily interact with P-selectin glycoprotein ligand-1 (PSGL-1) and Mac-1, triggering pro-inflammatory signaling and leukocyte recruitment (Merten et al., 1999). On endothelial cells, they engage adhesion molecules like ICAM-1 and integrins, promoting endothelial activation, pro-coagulant activity, and angiogenesis (Barry et al., 1998). These interactions are central to the progression of atherosclerosis, arterial thrombosis, and chronic inflammatory diseases such as rheumatoid arthritis (Boilard et al., 2010). Pharmacological targeting of these pathways involves the use of monoclonal antibodies to block specific adhesion molecules, such as Crizanlizumab, or the use of anti-platelet agents to reduce PEV formation (Ataga et al., 2017). While effective in reducing inflammatory and thrombotic risk, these interventions often carry a significant risk of bleeding due to the disruption of primary hemostasis (Coller, 1999).

Other names

Platelet-derived microvesicle receptorsPMV receptorspEV-cell surface interactorsP-selectin glycoprotein ligand-1 (PSGL-1)Intercellular adhesion molecule 1 (ICAM-1)Integrin alpha-M beta-2 (Mac-1)CD40 receptorLow-density lipoprotein receptor-related protein 1 (LRP1)

P-selectin inhibition, Integrin alpha-IIb beta-3 antagonism, Platelet activation inhibition, Blockade of vesicle-mediated cell-cell communication