Abstract
Extracellular vesicles (EVs), comprised of exosomes, microparticles, apoptotic bodies, and other microvesicles, are shed from a variety of cells upon cell activation or apoptosis. EVs promote clot formation, mediate pro-inflammatory processes, transfer proteins and miRNA to cells, and induce cell signaling that regulates cell differentiation, proliferation, migration, invasion, and apoptosis. This paper will review the contribution of EVs in hematological disorders, including hemoglobinopathies (sickle cell disease, thalassemia), paroxysmal nocturnal hemoglobinuria, and hematological malignancies (lymphomas, myelomas, and acute and chronic leukemias).
Highlights
EXTRACELLULAR VESICLESThere are millions of extracellular vesicles (EVs) in the circulation of healthy persons, and their level may increase in a variety of pathologies
This paper will review earlier studies which focus on the role of EVs in hematological disorders, including hemoglobinopathies, paroxysmal nocturnal hemoglobinuria, and hematological malignancies
Extracellular vesicles are detectable in the blood under normal physiological conditions, where their prevalence is increased in cases of cancer, inflammation, cardiovascular disease, diabetes, and preeclampsia.[1]
Summary
There are millions of extracellular vesicles (EVs) in the circulation of healthy persons, and their level may increase in a variety of pathologies. EVs modulate target cells by transferring proteins and miRNA to neighboring cells, elevating protein expression on the target cell membrane, and inducing cell signaling pathways that affect cell functions including differentiation, proliferation, migration, invasion, and apoptosis.[6,7,8,9] In addition, microparticles bearing coagulation and adhesion molecules, such as P-selectin and Pselectin glycoprotein ligand-1 (PSGL1), play a central role in coagulation initiation and thrombus formation.[10] Cell exposure to cytokines (tumor necrosis factor-alpha and interleukin-1) or chemotherapy results in microvesicle secretion.[11] Chemotherapy leads to platelet activation and generation of EVs associated with increased risk of thrombosis.[12] Additional triggers, such as complement cascade proteins,[13] states of hypoxia, irradiation, oxidative injury, or shear stress, increase the number of EVs shed by cells. The phosphatidylserine leaflet negative charge promotes membrane fusion and transfer of both proteins and lipids to other cells.[21]
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