State-of-the-Art-Review: Microvesicles in Blood Components: Laboratory and Clinical Aspects

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Abstract
There is ample evidence for the presence of microvesicles (MV) of different sizes and functions in various blood components. A variety of mechanisms have been proposed for the formation of MV. These include mechanical injury, shear stress, cell activation, activation of complements, hypoxia, and the cell aging process. While MV share many biological properties and surface receptors of their parental cells, they demonstrate significant differences in membrane asymmetry of the inner membrane phospholipid, in particular phosphatidylserine (PS). This provides high-affinity binding sites for the components of the prothrombinase complex. To what extent these MV contribute to hemostatic effectiveness, immudomodulation, and some untoward effects of the transfused blood components remains to be fully elucidated. Several methods for qualitative and semiquantitative characterization of MV are now available. Although in most cases it is necessary to separate MV from the intact cells for improved characterization, recent advances in flow cytometry make it possible to accurately differentiate MV in the presence of their parental cells on the basis of light scattering and fluorescent intensity. This review focuses on four main areas of MV in blood components: (1) the proposed mechanisms of platelet vesiculation, (2) factors influencing the formation of MV, (3) laboratory analysis of MV, and (4) the clinical impact of the presence of MV in blood components. Key Words: Microvesicte—Vesicutation—Biood component—Ptatelets—Transfusion.