Abstract
Endothelial microparticles (EMPs) are vesicles derived from cell membranes, which contain outsourced phosphatidylserine and express adhesion molecules, such as cadherin, intercellular cell adhesion molecule-1 (ICAM-1), E-selectin, and integrins. EMPs are expressed under physiological conditions and continue circulating in the plasma. However, in pathologic conditions their levels increase, and they assume a pro-inflammatory and pro-coagulant role via interactions with monocytes; these effects are related to the development of atherosclerosis. Chronic kidney dysfunction (CKD) characterizes this dysfunctional scenario through the accumulation of uremic solutes in the circulating plasma, whose toxicity is related to the development of cardiovascular diseases. Therefore, this review aims to discuss the formation of EMPs and their biological effects in the uremic environment. Data from previous research demonstrate that uremic toxins are closely associated with the activation of inflammatory biomarkers, cardiovascular dysfunction processes, and the release of EMPs. The impact of a decrease in circulating EMPs in clinical studies has not yet been evaluated. Thus, whether MPs are biochemical markers and/or therapeutic targets has yet to be established.
Highlights
Endothelial microparticles (EMPs) are vesicles derived from cell membranes, which contain outsourced phosphatidylserine and express adhesion molecules, such as cadherin, intercellular cell adhesion molecule-1 (ICAM-1), E-selectin, and integrins
EMPs derived from starved proteins have been reported by proteomics, some of which are cytosolic and some membranous, and cells transfer into a recipient cell, a functional microRNA-222 that can reduce the intercellular adhesion molecule (ICAM)-1 expression
The study did not exclude the possibility that high levels of EMPs in patients with uremia is a result of vascular diseases, since it is already well established that patients with Chronic kidney dysfunction (CKD) have an accelerated progression of atherosclerosis related to endothelial dysfunction [68]
Summary
Microparticles (MPs) were first described by Wolf in 1967 [1], when he observed a halo of debris surrounding activated platelets that he termed ‘platelet dust’. Lipid rafts have the function of organizing the proteins into microdomains, transduction of signals, and transport via caveolin This organization promotes the generation of unique responses resulting in the inclusion or exclusion of specific proteins and lipid species in cells, thereby explaining the different intravesicular compositions of MPs of the same cellular origin [6,11]. The release of MPs may induce cell signaling or may lead to the transfer of receptors between different cell types, since they carry parts of their cells of origin in their own membrane. EMPs may contribute directly and indirectly to the blood coagulation cascade through the tissue factor (TF) [19,20,21]
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