Air pollution‐associated procoagulant changes: the role of circulating microvesicles

Emmerechts, Jan; Jacobs, Lotte; kerckhoven, Soetkin Van; Loyen, Serena; Mathieu, Chantal; Fierens, Frans; Nemery, Benoît; Nawrot, Tim S.; Hoylaerts, Marc

doi:10.1111/j.1538-7836.2011.04557.x

Cited by 56 publications

(64 citation statements)

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“…The flow cytometry instrument settings and MP gating were adopted from previous works [2,12,16]. We used Megamix beads (BioCytex, Marseille, France) to determine the gate for MPs, as described previously [2,18]. Briefly, 0.5 μm, 0.9 μm and 3 μm beads were detected on an SSC/FL2 plot (Supplementary Fig.…”

Section: Flow Cytometric Analysis Of Pfp Samplesmentioning

confidence: 99%

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Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

György

Pálóczi

Kovacs

et al. 2014

Thrombosis Research

108

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Introduction: Recently extracellular vesicles (exosomes, microparticles also referred to as microvesicles and apoptotic bodies) have attracted substantial interest as potential biomarkers and therapeutic vehicles. However, analysis of microparticles in biological fluids is confounded by many factors such as the activation of cells in the blood collection tube that leads to in vitro vesiculation. In this study we aimed at identifying an anticoagulant that prevents in vitro vesiculation in blood plasma samples. Materials and Methods: We compared the levels of platelet microparticles and non-platelet-derived microparticles in platelet-free plasma samples of healthy donors. Platelet-free plasma samples were isolated using different anticoagulant tubes, and were analyzed by flow cytometry and Zymuphen assay. The extent of in vitro vesiculation was compared in citrate and acid-citrate-dextrose (ACD) tubes. Results: Agitation and storage of blood samples at 37°C for 1 hour induced a strong release of both platelet microparticles and non-platelet-derived microparticles. Strikingly, in vitro vesiculation related to blood sample handling and storage was prevented in samples in ACD tubes. Importantly, microparticle levels elevated in vivo remained detectable in ACD tubes. Conclusions: We propose the general use of the ACD tube instead of other conventional anticoagulant tubes for the assessment of plasma microparticles since it gives a more realistic picture of the in vivo levels of circulating microparticles and does not interfere with downstream protein or RNA analyses.© 2013 Elsevier Ltd. All rights reserved. IntroductionExtracellular vesicles (EVs) are membrane surrounded structures of various sizes (30-5000 nm) that have received significant attention recently [1]. EVs may be classified on the basis of their biogenesis, diameter and membrane markers. The two best characterized types of EVs include exosomes of endosomal origin and plasma membrane-derived microparticles (MPs) (recently often referred to also as microvesicles or ectosomes in the literature) [1]. EVs are present in all biological fluids including blood plasma, synovial fluid, cerebrospinal fluid, urine, tears and breast milk [1]. MPs are in between 100 and 1000 nm in diameter, and they are also detectable by flow cytometry [2,3]. Thus, MP profiles are easily analyzed in the routine clinical laboratory practice, and represent novel biomarkers of various diseases. In circulation, most MPs are derived from platelets, red blood cells, endothelial cells and leukocytes. Because of their abundance, platelet-derived MPs (PMPs) received the highest attention during the past few years. Elevated PMP counts are characteristic for nearly all autoimmune disorders [4,5], and also for several cardiovascular and metabolic diseases [1]. EVs not only contain proteins but also RNA molecules [1]. Extracellular RNA (exRNA) in blood plasma is encapsulated in EVs, or bound to either proteins or HDL molecules [6]. exRNAs, particularly miRNAs, are specific and sensitive biomarkers...

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Section: Flow Cytometric Analysis Of Pfp Samplesmentioning

confidence: 99%

“…2B). MP gate was set on the FSC/SSC plot as described previously [2,12,18] ( Supplementary Fig. 2B and C).…”

mentioning

confidence: 99%

Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

György

Pálóczi

Kovacs

et al. 2014

Thrombosis Research

108

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“…CS as well as PM exposure increases the release of phosphatidylserine (PS) + EV from different cell types in vitro and the concentrations of circulating PS + EV in vivo (Emmerechts et al 2012b;Li et al 2010;Neri et al 2016;Serban et al 2016). PS + EV may contribute to inflammation, as Serban et al (2016) reported that CSE-induced PS + EV from endothelial cells prevent efferocytosis of apoptotic cells by PS-dependent blocking of the phagocyte receptors for apoptotic cell engulfment.…”

Section: Interference With Efferocytosismentioning

confidence: 99%

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

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Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.

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“…Indeed prolonged exposure to air pollutans increases both the number of procoagulant vescicles and their procoagulant properties (Emmerechts J et al, 2012).…”

Section: Pathophysiological Mechanism Linking Particulate Matter (Pm)mentioning

confidence: 99%

Particulate matter phagocytosis induces tissue factor in differentiating macrophages

Milano

Dongiovanni

Artoni

et al. 2015

J of Applied Toxicology

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Airborne exposure to particulate matter with diameter < 10 mcM (PM10) has been linked to an increased risk of thromboembolic events, but the mechanisms are not completely understood. The aim of this study was to evaluate the effect of PM10 phagocytosis on the release of procoagulant molecules in human differentiating macrophages, and that of PM10 inhalation in an experimental model in rats. Human monocytes were separated from the peripheral blood by the lymphoprep method, differentiated in vitro and treated with standard PM10 or vehicle. Sprague–Dawley rats were instilled intratracheally with PM10 or vehicle alone. The outcome was expression of proinflammatory genes and of tissue factor (TF). In human differentiating macrophages, PM10 exposure upregulated inflammatory genes, but most consistently induced TF mRNA and protein levels, but not TF protein inhibitor, resulting in increased TF membrane expression and a procoagulant phenotype. Differentiation towards the anti‐inflammatory M2 phenotype inhibited PM10‐mediated TF expression. TF induction required phagocytosis of PM10, whereas phagocytosis of inert particles was less effective. PM10 phagocytosis was associated with a gene expression profile consistent with intracellular retention of iron, inducing oxidative stress. Both PM10 and iron activated the stress kinases ERK1/2 pathway, involved in the induction of TF expression. In rats, alveolar exposure to PM10 was associated with pulmonary recruitment of inflammatory cells and resulted in local, but not systemic, induction of TF expression, which was sufficient to increase circulating TF levels. In conclusion, TF induction by differentiating lung macrophages, activated following phagocytosis, contributes to the increased risk of thromboembolic complications associated with PM10 exposure. Copyright © 2015 John Wiley & Sons, Ltd.

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Air pollution‐associated procoagulant changes: the role of circulating microvesicles

Cited by 56 publications

References 50 publications

Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

Improved circulating microparticle analysis in acid-citrate dextrose (ACD) anticoagulant tube

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Particulate matter phagocytosis induces tissue factor in differentiating macrophages

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