Abstract

The formation of microvesicles by blood cells: monocytes, platelets, granulocytes, erythrocytes and endothelial cells is the most important feature of intercellular interactions. Red blood cells form microvesicles to remove damaged cell components, such as oxidized hemoglobin and damaged membrane components, and thus extend their functioning. Two hypotheses have been put forward for the formation of microvesicles: programmed cell death (eryptosis) and clustering of the band 3 protein as a result of disruption of intercellular interactions. In the process of eryptosis, damage to hemoglobin and a change in the pathways of phosphorylation of membrane proteins, primarily protein of strip 3, weaken the strong bonds between the lipid bilayer and the cytoskeleton, which is accompanied by the transformation of the membrane, the formation of protrusions and their transformation into microvesicles. It was found that the formation of microvesicles by red blood cells is impaired in patients suffering from various pathologies of red blood cells: sickle cell anemia, glucose-6-dehydrogenase deficiency, spherocytosis, and malaria. Studies of the last decade show that a violation of the interaction between the membrane and the cytoskeleton is probably the main mechanism, since it is confirmed by data obtained in the study of structural changes in red blood cells of donor hemocomponents stored in a blood bank. Currently, studies on the effect of microvesicles on the safety of erythrocyte-containing blood components have become widespread. A discussion was resumed on the relationship between the number of accumulated microvesicles in blood components and the effectiveness of donor components for patients during transfusion, depending on the shelf life of the components. Detailed data on proteomic, lipidomic and immunogenic comparisons of microvesicles obtained from various sources are convincing in the identification of trigger stimuli causing the generation of microvesicles. Elucidation of the contribution of microvesicles obtained from red blood cells to inflammation, thrombosis, and autoimmune reactions confirms the need to further study the mechanisms and consequences of the generation of microvesicles by red blood cells of donor components used for transfusion medicine.

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