Abstract
Red blood cells (RBCs) release extracellular vesicles (EVs) including both endosome-derived exosomes and plasma-membrane-derived microvesicles (MVs). RBC-derived EVs (RBCEVs) are secreted during erythropoiesis, physiological cellular aging, disease conditions, and in response to environmental stressors. RBCEVs are enriched in various bioactive molecules that facilitate cell to cell communication and can act as markers of disease. RBCEVs contribute towards physiological adaptive responses to hypoxia as well as pathophysiological progression of diabetes and genetic non-malignant hematologic disease. Moreover, a considerable number of studies focus on the role of EVs from stored RBCs and have evaluated post transfusion consequences associated with their exposure. Interestingly, RBCEVs are important contributors toward coagulopathy in hematological disorders, thus representing a unique evolving area of study that can provide insights into molecular mechanisms that contribute toward dysregulated hemostasis associated with several disease conditions. Relevant work to this point provides a foundation on which to build further studies focused on unraveling the potential roles of RBCEVs in health and disease. In this review, we provide an analysis and summary of RBCEVs biogenesis, composition, and their biological function with a special emphasis on RBCEV pathophysiological contribution to coagulopathy. Further, we consider potential therapeutic applications of RBCEVs.
Highlights
Publisher’s Note: MDPI stays neu-Extracellular vesicles (EVs) are a heterogenous population of membrane-delimited tral with regard to jurisdictional claims organelles released into the extracellular milieu by eukaryotic and prokaryotic cells [1].in published maps and institutional The first EV-like particles were suggested by Edward G
EVs in general are best known for their functions in intercellular communication, EV biogenesis and release have integral roles in Red blood cells (RBCs) maturation, ageing and disease
Increased circulating EVs may contribute toward hypercoagulability and thrombosis after refrigerator storage and are suggested to interfere with nitric oxide signaling, which leads to endothelial dysfunction as well as perfusion and oxygenation deficiency
Summary
Extracellular vesicles (EVs) are a heterogenous population of membrane-delimited tral with regard to jurisdictional claims organelles released into the extracellular milieu by eukaryotic and prokaryotic cells [1]. Proteomic analysis of exosomes derived from human cord blood reticulocytes as well as exosomes derived from human and murine reticulocytes has identified ESCRT proteins involved in MVB biogenesis These proteins— including Hrs (ESCRT-0), TSG101 (ESCRT-I), Alix (ESCRT-II), and CHMP4B (ESCRT-III)— highlight identical mechanisms of exosome biogenesis as described above [39,40]. These particular ESCRT proteins were identified in the human RBC proteome; their RBC specific roles in the process of vesiculation remains to be determined [41] and there remains a possibility that they represent carry over of EVs derived from nucleated cells
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