Tissue‐factor‐bearing microparticles (<scp>MP</scp>s‐<scp>TF</scp>) in patients with acute ischaemic stroke: the influence of stroke treatment on <scp>MP</scp>s‐<scp>TF</scp> generation

Świtońska, Milena; Słomka, Artur; Sinkiewicz, Włądysław; Żekanowska, Ewa

doi:10.1111/ene.12591

Cited by 33 publications

(36 citation statements)

References 39 publications

(51 reference statements)

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“…Therefore, elevated levels of circulating MPs and TF-loaded cMPs are associated with an increased risk of thrombosis and thromboembolic events. Recently it has been observed that in 73 patients with an acute ischemic stroke, TF-carrying cMPs were elevated compared to healthy individuals [ 26 ], in agreement with our findings. Besides, SMC shed TF-loaded MP with thrombogenic properties in human [ 27 ] and rat aorta [ 28 ].…”

Section: Discussionsupporting

confidence: 93%

Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke

Chiva‐Blanch¹,

Suades²,

Crespo³

et al. 2016

PLoS ONE

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PurposeIschemic stroke has shown to induce platelet and endothelial microparticle shedding, but whether stroke induces microparticle shedding from additional blood and vascular compartment cells is unclear. Neural precursor cells have been shown to replace dying neurons at sites of brain injury; however, if neural precursor cell activation is associated to microparticle shedding, and whether this activation is maintained at long term and associates to stroke type and severity remains unknown. We analyzed neural precursor cells and blood and vascular compartment cells microparticle shedding after an acute ischemic stroke.MethodsForty-four patients were included in the study within the first 48h after the onset of stroke. The cerebral lesion size was evaluated at 3–7 days of the stroke. Circulating microparticles from neural precursor cells and blood and vascular compartment cells (platelets, endothelial cells, erythrocytes, leukocytes, lymphocytes, monocytes and smooth muscle cells) were analyzed by flow cytometry at the onset of stroke and at 7 and 90 days. Forty-four age-matched high cardiovascular risk subjects without documented vascular disease were used as controls.ResultsCompared to high cardiovascular risk controls, patients showed higher number of neural precursor cell- and all blood and vascular compartment cell-derived microparticles at the onset of stroke, and after 7 and 90 days. At 90 days, neural precursor cell-derived microparticles decreased and smooth muscle cell-derived microparticles increased compared to levels at the onset of stroke, but only in those patients with the highest stroke-induced cerebral lesions.ConclusionsStroke increases blood and vascular compartment cell and neural precursor cell microparticle shedding, an effect that is chronically maintained up to 90 days after the ischemic event. These results show that stroke induces a generalized blood and vascular cell activation and the initiation of neuronal cell repair process after stroke. Larger cerebral lesions associate with deeper vessel injury affecting vascular smooth muscle cells.

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Section: Discussionsupporting

confidence: 93%

Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke

Chiva‐Blanch¹,

Suades²,

Crespo³

et al. 2016

PLoS ONE

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“…52–54 It has been shown that the level of brain damage is associated with the amount of TF that is released. 55,56 Also ischemic stroke patients have increased TF-bearing microparticles 57 and TF expression on monocytes. 58 …”

Section: Discussionmentioning

confidence: 99%

Contraction of Blood Clots Is Impaired in Acute Ischemic Stroke

Tutwiler

Peshkova

Andrianova

et al. 2017

ATVB

115

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Objective Obstructive thrombi or thrombotic emboli are the pathogenic basis of ischemic stroke. In vitro blood clots and in vivo thrombi can undergo platelet-driven contraction (retraction), resulting in volume shrinkage. Clot contraction can potentially reduce vessel occlusion and improve blood flow past emboli or thrombi. The aim of this work was to examine a potential pathogenic role of clot contraction in ischemic stroke. Approach and Results We employed a novel automated method that enabled us to quantify time of initiation, extent and rate of clot contraction in vitro. The main finding is clot contraction from the blood of stroke patients was reduced compared to healthy subjects. Reduced clot contraction correlated with a lower platelet count and their dysfunction, higher levels of fibrinogen and hematocrit, leukocytosis and other changes in blood composition that may affect platelet function and properties of blood clots. Platelets from stroke patents were spontaneously activated and displayed reduced responsiveness to additional stimulation. Clinical correlations with respect to severity and stroke etiology suggest that the impaired clot contraction has the potential to be a pathogenic factor in ischemic stroke. Conclusions The changeable ability of clots and thrombi to shrink in volume may be a novel unappreciated mechanism that aggravates or alleviates the course and outcomes of ischemic stroke. The clinical importance of clot or thrombus transformations in vivo and the diagnostic and prognostic value of this blood test for clot contraction needs further exploration.

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“…Higher TFMP levels have been demonstrated in patients with acute stroke, stable angina, and acute myocardial infarction (AMI) as compared with healthy subjects. [57][58][59] Conversely, two other studies found that AMI patients had in fact lower TFMP levels than controls. 60,61 These authors hypothesized that adherence of TFMP to the coronary thrombus might lead to a decreased number of circulating TFMP, which is in line with earlier findings of increased levels of TFMP within occluded coronary arteries compared with peripheral blood.…”

Section: Tf-exposing Mp and Arterial Thrombosismentioning

confidence: 99%

Clinical Significance of Tissue Factor–Exposing Microparticles in Arterial and Venous Thrombosis

Bleker

Sturk

et al. 2015

Semin Thromb Hemost

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Microparticles (MP) are small extracellular vesicles (30-1,000 nm) that are released from activated cells or platelets. Exposure of negatively charged phospholipids and tissue factor (TF) renders MP procoagulant. Normal plasma levels of intravascular TF-exposing MP (TFMP) are low, but their number may rise in pathological conditions, including cancer and infectious disease. Emerging evidence indicates an important role for these circulating TFMP in the pathogenesis of thrombotic complications such as venous thromboembolism and disseminated intravascular coagulation, whereas their contribution to arterial thrombosis is less studied. Despite serious limitations of the currently available assays for measuring TFMP levels or the procoagulant activity associated with TFMP with respect to sensitivity and specificity, the scientific interest in TFMP is rapidly growing because their application as prognostic biomarkers for thrombotic complications is promising. Future advances in detection methods will likely provide more insight into TFMP and eventually improve their clinical utility.

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Tissue‐factor‐bearing microparticles (MPs‐TF) in patients with acute ischaemic stroke: the influence of stroke treatment on MPs‐TF generation

Abstract: Our findings suggest that patients with acute ischaemic stroke have increased generation of MPs-TF. Nevertheless, further studies are needed in order to confirm such inference.

Cited by 33 publications

References 39 publications

Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke

Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke

Contraction of Blood Clots Is Impaired in Acute Ischemic Stroke

Clinical Significance of Tissue Factor–Exposing Microparticles in Arterial and Venous Thrombosis

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