Endothelial cells (ECs) have long been implicated in the pathogenesis and pathophysiology of a myriad of vascular, thrombotic, and inflammatory disorders [1-3]. The prevalence of endothelial perturbation in vascular disease has underscored the need for noninvasive sensitive and specific markers to monitor endothelial status . The popularity of endothelial microparticles (EMPs) as markers of perturbed has increased because of its promising clinical applications in the area of noninvasive EC monitoring . This trend can be attributed to a significant increase in the information available about EMPs' role in health and disease and their presence in different disorders . Concomitant with this wealth of information, new challenges have risen to the fore. Perhaps the most crucial, and most decidedly relevant to the field of clinical laboratory testing, has been the issue of methodology [5, 6]. Indeed, to this day, there is no consensus about which is the best protocol to determine EMP, and a number of different flow cytometric and immunologic methods with several variations have been adopted . This review introduces the methodologies currently employed in the area of clinical EMP research. Moreover, issues that may have an effect on the clinical application of EMP assays are also discussed.
"variety of vascular disease states (Jimenez et al. 2005). Not only are EMP capable of rapid binding to monocytes through association with monocyte b 2 integrins, but also, in other instances , monocyte–microparticle interactions in vitro promote increased expression of adhesion receptors on both monocytes and endothelial cells to facilitate cellular adhesion (Sabatier et al. 2002; Barry et al. 1998). "
[Show abstract][Hide abstract] ABSTRACT: High-fat meals promote transient increases in proatherogenic factors, implicating the postprandial state in cardiovascular disease (CVD) progression. Although low-grade inflammation is associated with CVD, little research has assessed postprandial inflammation. Because of its anti-inflammatory properties, premeal exercise may counteract postprandial inflammation. The purpose of this study was to determine postprandial alterations in monocytes and circulating markers of endothelial stress and inflammation following a high-fat meal in young adults with or without premeal cycle exercise. Each subject completed two trials and was randomized to rest or cycle at a moderate intensity prior to eating a high-fat meal. Flow cytometry was used to assess monocyte cell surface receptor expression and concentration of endothelial microparticles (EMP). Plasma cytokines were assessed using Luminex MagPix. Statistical analysis was completed using separate linear mixed models analyses with first-order autoregressive (AR(1)) heterogeneous covariance structure. Significance was set at P ≤ 0.05. Percentage increases in classic monocyte CD11a and CD18 were greater overall in the postprandial period in the meal-only condition compared with the meal + exercise condition (P < 0.05). EMP concentration was 47% greater 3 h after the meal compared with premeal values in the meal-only condition (P < 0.05); no significant increase was observed in the meal + exercise condition. Premeal cycling blunted postprandial increases in EMP and CD11a and CD18. Acute, moderate-intensity exercise may help counteract possibly deleterious postprandial monocyte and endothelial cell activation.
"However, the postprandial perturbations observed in this study are likely to be relevant to clinical risk. CD31+/42b¡ EMP have been shown to be elevated in a number of vascular disease states (Jimenez et al. 2005) and to distinguish high and low risk coronary lesions (Bernal-Mizrachi et al. 2004). The postprandial increases in EMP, in both the control and exercise trials are indicative of postprandial endothelial activation. "
[Show abstract][Hide abstract] ABSTRACT: Triglyceride-rich postprandial lipoproteins are known to activate endothelial cells in vitro, contributing to atherosclerosis. Endothelial microparticles (EMP) are membranous vesicles released into the circulation from vascular endothelial cells that permit cell activation to be monitored in vivo. The objective of the study was to examine changes in EMP following a high fat meal, consumed with and without prior exercise. Eight recreationally active young men underwent two oral fat tolerance tests following either 100 min exercise at 70% VO(2)peak (EX trial) or no exercise (CON trial) on the previous evening. Postprandial triglycerides were reduced (1.97 +/- 0.31 vs. 1.17 +/- 0.13 mmol L(-1), p < 0.05) and HDL-cholesterol (HDL-C) increased (1.20 +/- 0.07 vs. 1.30 +/- 0.08 mmol L(-1), p < 0.05) in the EX compared to CON trial. EMP (CD31+/42b-) increased postprandially (p < 0.05). However, counts were not different between trials (postprandial CON and EX trial counts x 10(3 )microL(-1), 3.10 +/- 0.14 vs. 3.26 +/- 0.37). There were no changes in sICAM-1 or sVCAM-1 postprandially and no differences between trials. Interleukin-6 (IL-6) and leukocytes increased postprandially (p < 0.05). IL-6 values were not different between trials. Leukocytes were higher at 0 h in the EX trial with CON and EX trial values similar at 6 h. EMP, but not sICAM-1 or sVCAM-1, increase in response to a high fat meal. However, EMP are not attenuated by acute exercise, despite a considerable reduction in postprandial lipemia and an increase in HDL-C.
[Show abstract][Hide abstract] ABSTRACT: We studied the levels of endothelial microparticles (EMPs), IL-6, and TNF-α in patients with Kawasaki disease (KD). EMPs were enumerated by flow cytometry, while IL-6 and TNF-α were measured using enzyme-linked immunosorbent assay. EMPs and IL-6 were elevated in KD, the level of TNF-α in KD was not different from disease controls, but higher than healthy controls. EMPs were positively correlated with TNF-α and negatively correlated with albumin. Elevated level of EMPs, a biomarker of endothelial cells damage, concomitant with increased levels of TNF-α and IL-6, is seen in patients with KD.
Indian pediatrics 05/2013; 50(5). DOI:10.1007/s13312-013-0152-7 · 1.04 Impact Factor
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