Red Blood Cell Microparticles: Clinical Relevance

Rubin, Olivier; Canellini, Giorgia; Delobel, Julien; Lion, Niels; Tissot, Jean‐Daniel

doi:10.1159/000342228

Cited by 68 publications

(56 citation statements)

References 46 publications

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“…Most microvesicles in the systemic circulation originate from platelets [ 26 ] but they may originate from a variety of cells, including leukocytes [ 27 ], red blood cells [ 28 ] and endothelial cells [ 29 ]. As they transport substances derived from the cell of origin they may contain a broad spectrum of receptors, DNA, mRNA, micro RNA, histones and other proteins, as well as lipids capable of interacting with cells.…”

Section: Microvesiclesmentioning

confidence: 99%

Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions

Karpman

Ståhl

Arvidsson

et al. 2015

Advances in Experimental Medicine and Biology

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The complement system is activated in the vasculature during thrombotic and inflammatory conditions. Activation may be associated with chronic inflammation on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting inflammation and thrombosis. Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are small membrane vesicles ranging from 0.1 to 1 μm, shed by cells during activation, injury and/or apoptosis that express components of the parent cell. Microvesicles are released during inflammatory and vascular conditions. The repertoire of inflammatory markers on endothelial cell-derived microvesicles shed during inflammation is large and includes complement. These circulating microvesicles may reflect the ongoing inflammatory process but may also contribute to its propagation. This overview will describe complement activation on blood and endothelial cells and the release of microvesicles from these cells during hemolytic uremic syndrome, thrombotic thrombocytopenic purpura and vasculitis, clinical conditions associated with enhanced thrombosis and inflammation.

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Section: Microvesiclesmentioning

confidence: 99%

Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions

Karpman

Ståhl

Arvidsson

et al. 2015

Advances in Experimental Medicine and Biology

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“…18–23 MP release from platelets,24 red blood cells,25 endothelial cells, tumor cells,26,27 and leucocytes28 has been reported. Because MPs are shed membrane vesicles, the antigens expressed on the original cells are expressed on the membrane of the MPs.…”

Section: Mpsmentioning

confidence: 98%

The role of microparticles in chronic obstructive pulmonary disease

Takahashi¹,

Kubo²

2014

COPD

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Accumulating evidence suggests that cell injury in lung tissues is closely connected to disease progression in chronic obstructive pulmonary disease (COPD). Microparticles (MPs) are shed membrane vesicles that are released from platelets, leukocytes, red blood cells, and endothelial cells when these cells are activated or undergo apoptosis under inflammatory conditions. Based on increasing evidence that endothelial injury in the pulmonary capillary vasculature leads to lung destruction, and because cardiovascular diseases are the main cause of death among individuals with COPD, endothelial MPs (EMPs) are now receiving attention as potential biomarkers for COPD. There are eight types of EMPs which are defined by the presence of different endothelial markers on the cell membrane: vascular endothelial-cadherin; platelet endothelial cell adhesion molecule; melanoma cell adhesion molecule; E-selectin; CD51; CD105; von Willebrand factor; and CD143 EMPs. Vascular endothelial-cadherin, platelet endothelial cell adhesion molecule, and E-selectin EMPs are increased in patients with stable COPD and are further increased in patients with exacerbated COPD compared to non-COPD patients. In addition, the levels of these three EMPs in patients with stable COPD are significantly correlated with lung destruction and airflow limitation. These results indicate that endothelial injury is closely connected to the pathophysiology of COPD. Interestingly, the variations in the levels of the eight EMP subtypes were not identical with changes in patient condition. Although the clinical significance of the differences in these eight EMP subtypes remains unclear, evaluating the expression pattern of endothelial antigens on circulating MPs might predict the presence and degree of endothelial injury in COPD patients. In addition, circulating MPs are proposed to have several physiological functions in vivo, such as intercellular crosstalk; the increase in EMPs in COPD seems to play a role in the pathophysiology of this disease.

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“…Most studies have shown that microparticles are heterogeneous and vary in phospholipids, surface antigens, and protein contents. MP release is a controlled process triggered by various stimuli including proapoptotic stimulation, shear stress, agonists, or damage [6]. By general consensus, MPs are small in size, expose the anionic phospholipid (PL) phosphatidylserine (PS) on the outer leaflet of their membrane, and bear surface membrane antigens reflecting their cell of origin [7].…”

Section: Microparticlesmentioning

confidence: 99%