Transfer of Tissue Factor from Platelets to Monocytes: Role of Platelet-Derived Microvesicles and CD62P

Scholz, Thomas; Temmler, Uta; Krause, S.; Heptinstall, Stan; Lösche, Wolfgang

doi:10.1055/s-0037-1613351

Cited by 109 publications

(80 citation statements)

References 15 publications

(20 reference statements)

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“…Although some smaller MVs might not be captured in a flow cytometric approach, we detected MVs from all major blood cell populations (e.g., platelets, red blood cells, leukocytes, endothelial cells). In our analyses we used standard markers for the different blood cells that have been previously found on MVs [26][27][28][29] . It should be noted that in order to obtain the best possible results by flow cytometry, the amount and concentration of all antibodies should be titrated on a MV sample expressing the antigen of interest.…”

Section: Discussionmentioning

confidence: 99%

Isolation and Characterization of Microvesicles from Peripheral Blood

Menck

Bleckmann

Schulz

et al. 2017

JoVE

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The release of extracellular vesicles (EVs) including small endosomal-derived exosomes (Exos, diameter < 100 nm) and large plasma membrane-derived microvesicles (MVs, diameter > 100 nm) is a fundamental cellular process that occurs in all living cells. These vesicles transport proteins, lipids and nucleic acids specific for their cell of origin and in vitro studies have highlighted their importance as mediators of intercellular communication. EVs have been successfully isolated from various body fluids and especially EVs in blood have been identified as promising biomarkers for cancer or infectious diseases. In order to allow the study of MV subpopulations in blood, we present a protocol for the standardized isolation and characterization of MVs from peripheral blood samples. MVs are pelleted from EDTA-anticoagulated plasma samples by differential centrifugation and typically possess a diameter of 100 -600 nm. Due to their larger size, they can easily be studied by flow cytometry, a technique that is routinely used in clinical diagnostics and available in most laboratories. Several examples for quality control assays of the isolated MVs will be given and markers that can be used for the discrimination of different MV subpopulations in blood will be presented.

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Section: Discussionmentioning

confidence: 99%

Isolation and Characterization of Microvesicles from Peripheral Blood

Menck

Bleckmann

Schulz

et al. 2017

JoVE

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“…Blood plasma has been shown to contain microparticles (38,41), a subfraction of which contains active TF thought to be derived from platelets. The transfer of such microparticles from platelets to plaque macrophages has also been proposed to explain the rapid accumulation of TF in activated plaques (55). However, the notion of blood-borne TF in general, and as an integral component of platelets or of mononuclear cells in blood in particular, is in conflict with recent data suggesting that rather the platelets may be important in decrypting monocyte TF activity in a process entailing transfer of TF from these cells to activated platelets (11,46,47).…”

Section: Discussionmentioning

confidence: 99%

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

Juchem¹,

Weiss

Gansera

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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The frequently observed de-endothelialization of venous coronary bypass grafts prepared using standard methods exposes subendothelial prothrombotic cells to blood components, thus endangering patients by inducing acute thromboembolic infarction or long-term proliferative stenosis. Our aim was to gain deeper histological and physiological insight into these relations. An intricate network of subendothelial cells, characterized by histological features specific for true pericytes, was detected even in healthy vessels and forms, coupled to the luminal endothelium, a second leaflet of the macrovascular intima. These cells, and particularly those in the venous intima, express enormous concentrations of tissue factor and can recruit additional amounts of up to the 25-fold concentration within 1 h during preincubation with serum (intimal pericytes of venous origin activate 30.71 ± 4.07 pmol coagulation factor x·min−1·10−6 cells; n = 15). Moreover, decoupled from the endothelium, they proliferate rapidly (generation time, 15 ± 2.1 h, n = 8). Central regions of atherosclerotic plaques, as well as of those of restenosed areas of coronary vein grafts, consist almost completely of these cells. In stark contrast with the prothrombogenicity of the intimal pericytes, intact luminal endothelium recruits high concentrations of thrombomodulin (CD 141) specifically within its intercellular junctions, activates Protein C rapidly (42 ± 5.1 pmol/min·106 venous endothelial cells at thrombin saturation; n = 15), can thus actively prevent coagulatory processes, and never expresses histologically detectable and functionally active tissue factor. Given this strongly prothrombotic potential of the intimal pericytes and their overshooting growth behavior in endothelium-denuded vascular regions, they may play important roles in the development of atherosclerosis, thrombosis, and saphenous vein graft disease.

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“…Monocytes are known to exchange microparticles-bound TF with platelets and because megakaryocytes do not express TF, it is likely that this exchange represents a mechanism through which platelets are loaded with TF (Scholz T et al, 2002).…”

Section: Tissue Factor (Tf)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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Transfer of Tissue Factor from Platelets to Monocytes: Role of Platelet-Derived Microvesicles and CD62P

Cited by 109 publications

References 15 publications

Isolation and Characterization of Microvesicles from Peripheral Blood

Isolation and Characterization of Microvesicles from Peripheral Blood

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

Particulate matter phagocytosis induces tissue factor in differentiating macrophages

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