2001
DOI: 10.1212/wnl.56.10.1319
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Elevated plasma endothelial microparticles in multiple sclerosis

Abstract: Endothelial dysfunction is evident during exacerbation of MS, evidenced by shedding of EMP expressing PECAM-1 (CD31). The in vitro data indicate contribution of one or more plasma factors in endothelial dysfunction of MS.

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Cited by 273 publications
(254 citation statements)
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“…To assess endothelial cell injury in response to superantigen-dependent T cell-mediated activation, EMPs released by HUVECs into the supernatant for each of the different experimental conditions were measured using flow cytometry. EMPs were de- fined as particles smaller than 1.5 m that bound annexin V (and hence, expressed the negatively charged phospholipid phosphatidylserine) and expressed the endothelial surface markers E-selectin, CD105, ICAM-1, or VCAM-1, as previously described (11,18,19). TNF␣ again served as a positive control in these experiments.…”
Section: Resultsmentioning
confidence: 99%
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“…To assess endothelial cell injury in response to superantigen-dependent T cell-mediated activation, EMPs released by HUVECs into the supernatant for each of the different experimental conditions were measured using flow cytometry. EMPs were de- fined as particles smaller than 1.5 m that bound annexin V (and hence, expressed the negatively charged phospholipid phosphatidylserine) and expressed the endothelial surface markers E-selectin, CD105, ICAM-1, or VCAM-1, as previously described (11,18,19). TNF␣ again served as a positive control in these experiments.…”
Section: Resultsmentioning
confidence: 99%
“…The morphologic characteristics of EMPs by electron microscopy have been well described by Combes et al (11). It is now becoming apparent that EMPs provide a window to the activated endothelium in a number of disease states in which endothelial injury is central to the disease process, including atherosclerosis (16), acute coronary syndromes (17), antiphospholipid syndrome (APS) (11), thrombotic thrombocytopenic purpura (TTP) (18), multiple sclerosis (MS) (19), and most recently, hypertension (20) in adults. Moreover, plasma from patients with APS, MS, or TTP was shown to induce the formation of EMPs from endothelial cells in tissue culture (11,18,19).…”
Section: Methodsmentioning
confidence: 99%
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“…The chronic inflammatory environment in RRMS (Lund et al, 2004) probably underlies this inappropriate neutrophil priming, which may result in enhanced neutrophil activation during infection. The higher levels of NETs in serum might also be linked to the chronic inflammatory environment in MS, but may have been caused by other triggers such as infections, that have been associated with relapses in these patients (Granieri et al, 2001) or higher frequency of activated platelets (Sheremata et al, 2008) or endothelial cells (Minagar et al, 2001) both elevated in MS. Due to the central role of T cells in RRMS and the ability of NETs to modulate T cell immunity, an abnormally gender-specific high level of NETs in this disease as consequence of neutrophil priming may play an important role in certain aspects of the pathogenesis and also explain some gender-specific differences.…”
Section: -Introductionmentioning
confidence: 99%
“…Their plasma levels are elevated in many pathological conditions, including lupus, acute coronary syndrome, diabetes, sepsis, and multiple sclerosis. [1][2][3][4][5] MPs were discovered as a component of the blood which promoted coagulation due to the presence of anionic phospholipids on their outer surface, 6 and have traditionally been viewed as markers of cellular activation and/or damage generated by the random blebbing of cell membranes. However, MPs contain a unique subset of proteins derived from the parent cell, [7][8][9] and in recent years it has become clear that MPs have important biological functions.…”
Section: Introductionmentioning
confidence: 99%