Evaluation of Factors Associated With Elevated Levels of Platelet-Derived Microparticles in the Acute Phase of Cerebral Infarction (original) (raw)
Platelet activation and reactivity in the convalescent phase of ischaemic stroke
Thrombosis and Haemostasis, 2010
SummaryThe study was aimed at the evaluation of blood platelet activation and reactivity in patients in the convalescent phase of stroke (n=58) and controls matched in respect to risk factors of vascular pathology (n=55). Both groups were treated daily with acetylsalicylic acid (ASA), 150 mg/day. Using flow cytometry, the expressions of P-selectin and the active GP IIb/IIIa receptor, as well as the fraction of platelet-derived microparticles (PMPs) and total platelet aggregates (Ag), were evaluated in non-stimulated platelets and in platelets stimulated in vitro by thrombin, thrombin receptor activating peptide (TRAP) or ADP. The expression of P-selectin in non-stimulated platelets was found to be significantly (p=0.04) lower in stroke patients. In parallel, these patients manifested a significantly (p=0.0008) higher proportion of PMPs and a lowered (p=0.003) proportion of Ag, as compared to the controls. In the stroke patients the increased expressions of P-selectin and active GP I...
Potential roles of cell-derived microparticles in ischemic brain disease
Neurological Research, 2009
The objective of this study is to review the role of cell-derived microparticles in ischemic cerebrovascular diseases. Materials and methods: An extensive PubMed search of literature pertaining to this study was performed in April 2009 using specific keyword search terms related to cell-derived microparticles and ischemic stroke. Some references are not cited here as it is not possible to be all inclusive or due to space limitation. Discussion: Cell-derived microparticles are small membranous vesicles released from the plasma membranes of platelets, leukocytes, red cells and endothelial cells in response to diverse biochemical agents or mechanical stresses. They are the main carriers of circulating tissue factor, the principal initiator of intravascular thrombosis, and are implicated in a variety of thrombotic and inflammatory disorders. This review outlines evidence suggesting that cell-derived microparticles are involved predominantly with microvascular, as opposed to macrovascular, thrombosis. More specifically, cell-derived microparticles may substantially contribute to ischemic brain disease in several settings, as well as to neuroinflammatory conditions. Conclusion: If further work confirms this hypothesis, novel therapeutic strategies for minimizing cell-derived microparticles-mediated ischemia are available or can be developed, as discussed.
Brain Research, 2020
Limited lower detection ranges associated with traditional immunoassay techniques have prevented the use of brain-specific proteins as blood biomarkers of stroke in the acute phase of care, as these proteins are often only present in circulation at low concentrations. Digital ELISA is a newly developed technique with allows for quantification of proteins in biofluids with up to 1000 times greater sensitivity than conventional ELISA techniques. The purpose of this study was to determine whether the extended lower limits of detection associated with digital ELISA could enable the use of brain-specific proteins as blood biomarkers of ischemic stroke during triage. Blood was sampled from ischemic stroke patients (n=14) at emergency department admission, as well as from neurologically normal controls matched in terms of risk factors for cardiovascular disease (n=33). Plasma levels of two brain-specific axonal proteins, neurofilament light chain (NfL) and Tau, were measured via digital ELISA, and receiver-operator characteristic analysis was used to determine their ability to discriminate between groups. Plasma levels of NfL and Tau were both significantly elevated in stroke patients versus controls, and could respectively discriminate between groups with 92.9% sensitivity and 84.9% specificity, and 85.7% sensitivity and 54.6% specificity. Furthermore, adjustment of measured NfL and Tau levels according to the lower-limits of detection associated with commercially-available conventional ELISA assays resulted in a dramatic and statistically significant decrease in diagnostic performance. Collectively, our results #
Clinical and Applied Thrombosis/Hemostasis, 2011
An upregulation of platelet CD40 ligand (CD40L) and CD62P has been described in atherosclerotic cardiovascular diseases and among patients with acute cerebral ischemia. Correlation between platelet and monocyte activation and the etiology of ischemic stroke were examined in 41 patients with acute ischemic stroke. Compared to 10 controls, all patients with stroke showed a significantly elevated platelet expression of CD40L ( P < .001) and had significantly higher amounts of platelet–monocyte aggregates ( P = .002). Plasma levels of interleukin 7 were significantly lower in patients with stroke compared to controls ( P = .006). Patients with small artery disease had a significantly higher platelet CD40L expression than patients with cardioembolic stroke ( P = .029). Plasma levels of soluble CD40L were significantly higher in patients with large artery disease compared to patients with cardioembolic stroke ( P = .047). In conclusion, patients with acute ischemic stroke show an upreg...
Predictive Markers of Blood Cytokine and Chemokine in Recurrent Brain Infarction
Journal of Interferon & Cytokine Research, 2009
The mechanism of the infl ammatory response in the vascular wall in atherothrombosis and during the progression of atherosclerosis has attracted attention. We focused on the potential usefulness of infl ammatory markers in chronic recurrent brain infarction, and analyzed the role of infl ammatory markers in atherosclerosis of the intracranial artery. The subjects were 2 groups of patients treated between 2004 and 2006: a group of outpatients with recurrent infarction (group RI), who developed atherothrombotic brain infarction twice; another group of outpatients with brain infarction without recurrence (group BI), who developed brain infarction once and remained free of recurrence for >1 year; and a group of control subjects with normal brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) (group C). Plasma samples were collected from each group of patients for the simultaneous measurement of 17 kinds of candidate infl ammatory markers, using a fl uorescent microbead array system, and the results were compared with head MRA fi ndings. The levels of high-sensitivity C-reactive protein (hsCRP) and monocyte chemoattractant protein-1 (MCP-1) were signifi cantly higher in group RI patients than in groups C and BI. Subjects with a hsCRP level ≥0.3 and a MCP-1 level ≥200 in the serum have, respectively, a 1.92 and 2.98 relative risk to have a potential recurrent infarction. Regarding the relation of infl ammatory marker levels with MRA fi ndings, group RI showed signifi cantly higher levels of hsCRP at M1 lesions and MCP-1 at A1 and M1 lesions than group BI (P < 0.05). In conclusion, the MCP-1 level as well as hsCRP in the blood can be a potential predictive marker of recurrent thrombotic brain infarction, and may refl ect infl ammation that promotes intracranial large-artery atherosclerosis.
British Journal of Haematology, 2001
Endothelial injury is believed to be a key initiating event in the pathogenesis of thrombotic thrombocytopenic purpura (TTP), leading to platelet activation and formation of platelet-rich thrombi in microvasculature. However, the nature of endothelial injury in TTP is poorly defined and clinical assays to rapidly and reliably monitor endothelial damage are not readily available. Using flow cytometry, we measured endothelial microparticles (EMPs) generated from cultured renal and brain microvascular endothelial cells (MVECs) during activation and apoptosis, and evaluated the effect of TTP plasma on them. EMPs were measured using positivity for monoclonal antibodies (mAbs) CD31 and CD51, and their procoagulant activity was assessed using a Russell viper venom assay. Both cell lines generated procoagulant EMPs when cultured with inducers of activation (tumour necrosis factor alpha; TNF-a) or apoptosis (mitomycin C). TTP plasma induced a five-to sixfold increase of EMP generation and a two-to threefold increase of procoagulant activity in cultured brain and renal MVECs. TTP plasma induced a threefold and 13-fold increase of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression, respectively, on renal MVECs. Procoagulant activity tended to parallel EMP numbers. The effect of TTP plasma on cell viability was similar to that of TNF-a, implying that it induced activation rather than apoptosis. Control plasma and idiopathic thrombocytopenic purpura (ITP) plasma had little effect. In the clinical study, EMP assay of blood from acute TTP patients showed levels markedly elevated compared with normal controls, but values returned to normal in remission. In conclusion, TTP plasma activated and induced injury to MVECs in culture, judged by production of EMP and expression of activation markers. Released procoagulant EMP may play a role in the pathogenesis of TTP. Assay of EMP may be a useful marker of disease activity and endothelial injury in TTP and possibly other thrombotic disorders.
Correlation between platelet counts, MPV, PDW, PCT and age in acute ischemic stroke patients
Medical Laboratory Journal, 2024
Background: Acute ischemic stroke occurs when blood clots obstruct blood vessels within the brain. Platelets (Plts) are integral to the pathophysiology of stroke. This research aimed to explore the relationship between Plt quality and Plt indices in the context of acute ischemic stroke. Methods: This cross-sectional investigation involved 100 patients diagnosed with acute ischemic stroke at Kosti Teaching Hospital and Alyammama Hospitals. The diagnosis was confirmed using brain CT imaging and electrocardiography (ECG). Blood samples were collected in EDTA-containing tubes within 24 hours following the commencement of treatment and were subsequently analyzed for Plt count, mean Plt volume (MPV), Plt distribution width (PDW), and plateletcrit (PCT) utilizing a hematological analyzer. Data were analyzed using GraphPad Prism software. Results: Platelet counts negatively correlated with PDW [r=-0.074, P=0.459; R=-0.023, P=0.815], MPV [r=-0.130, P=0.194; R=-0.081, P=0.417], and diastolic blood pressure [r= -0.023, P=0.818; R= -0.024, P=0.805]; and positively correlated with PCT [r= 0.103, P=0.308; R=0.143, P=0.155] and diastolic blood pressure [r=0.022, P=0.823; R= 0.008, P=0.932]. Moreover, PDW positively correlated with systolic blood pressure [r=0.105, P=0.298; R= 0.147, P=0.148] and diastolic blood pressure [r=0.146, P=0.145; R=0.173, P=0.084]. Based on Spearman but not Pearson correlation, PDW showed a negative correlation with PCT [r=-0.005, P=0.959; R=0.010, P=0.929]. Conclusion: The study shows a correlation between Plt count and indices in ischemic stroke patients. The research also presented evidence concerning the relationship between diastolic and systolic blood pressure and Plt counts and indices.