P-selectin and platelet-derived microparticles associated with monocyte activation markers in patients with pulmonary embolism.
ABSTRACT Platelet activation markers (platelet-derived microparticles and P-selectin on activated platelets), chemokines (monocyte chemotactic peptide and regulated on activation normally T-cell expressed and secreted), and soluble markers (sP-selectin, sE-selectin, sVCAM-1, and sCD14) were measured and compared in patients with pulmonary embolism (PE). These substances are thought to participate in the pathogenesis of PE. Levels of all of the platelet activation markers, chemokines, and soluble markers were higher in the patients with PE than in normal controls. Levels of platelet activation markers were also significantly increased postoperatively after total knee arthroplasty. Anti-platelet therapy significantly inhibited the elevation of platelet activation markers after total knee arthroplasty. These findings suggest that antiplatelet therapy may be useful for PE-related interaction of platelets, leukocytes, and endothelial cells.
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ABSTRACT: Abnormal thrombus formation and resolution underlie many vascular disorders, including venous thromboembolism (VTE), stroke, hypertension, and myocardial infarction. Conditions that account for both venous and arterial thrombosis such as the antiphospholipid antibody syndrome, hyperhomocysteinemia, malignancies, infections, and hormone treatment provide a pathophysiological link between arterial and venous thrombosis. Furthermore, recent trials have demonstrated that patients with VTE are at increased risk of arterial thrombosis. The scope of this chapter is to define the characteristics of venous thrombosis and VTE, the role of soluble factors, and to emphasize the role of the vascular wall and of circulating cells, thus creating a new view of thrombosis, beyond classic coagulation and fibrinolysis.Pulmonary circulation. 12/2013; 3(4).
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ABSTRACT: Microparticles (MPs) are small fragments of apoptotic or activated cells that may contribute to pathological processes in cardiovascular diseases. In studies of MPs in clinical cohorts, it is unclear if observed changes in MP composition are a cause or a result of the cardiovascular disease being studied. The present studies employed a well-characterized rat model of experimental pulmonary embolism (PE) to determine if there were changes in MP characteristics as a result of pulmonary vascular occlusion. PE was produced by infusing 25 μm polystyrene microspheres into the jugular vein of anesthetized rats. MPs were isolated by differential centrifugation of arterial blood 18 hr after PE. Proteins were separated by 1D gel electrophoresis and identified from tryptic digests by ultraperformance liquid chromatography (UPLC) coupled with tandem mass spectrometry. Statistical analysis was conducted using the Power Law Global Error Model (PLGEM). Changes in two proteins were confirmed by Western blot. Experimental PE produced pulmonary hypertension, mild systemic hypotension, hypoxia, hypercapnia and lactic acidosis. MPs showed significant elevation in proteins involved in clotting (fibronectin precursor, fibrinogen alpha, beta and gamma and von Willebrand factor) and several macroglobulin proteins, such as alpha-2-macroglobulin precursor compared with vehicle-treated control rats. Consistent with recent observations of hemolysis in PE, haptoglobin precursor protein, a major protein of hemoglobin clearance, decreased significantly in the PE animals. Plasma d-Dimer concentrations were significantly elevated, indicating that experimental PE produced a pro-coagulant state. These findings suggest that experimental PE produced significant, changes in MP characteristics to a prothrombotic phenotype.Thrombosis Research 10/2011; 130(1):122-8. · 3.13 Impact Factor
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ABSTRACT: There is evidence that inflammatory bowel diseases (IBD) combine both inflammation and coagulation in their pathogenesis and clinical manifestations. Although platelets (PLT) are well known for their role in hemostasis, there are a rising number of studies supporting their considerable role as inflammatory amplifiers in chronic inflammatory conditions. IBD are associated with several alterations of PLT, including number, shape, and function, and these abnormalities are mainly attributed to the highly activated state of circulating PLT in IBD patients. When PLT activate, they increase in size, release a great variety of bio-active inflammatory and procoagulant molecules/particles, and express a variety of inflammatory receptors. These inflammatory products may represent a part of the missing link between coagulation and inflammation, and can be considered as possible IBD pathogenesis instigators. In clinical practice, thrombocytosis is associated both with disease activity and iron deficiency anemia. Controlling inflammation and iron replacement in anemic patients usually leads to a normalization of PLT count. The aim of this review is to update the role of PLT in IBD and present recent data revealing the possible therapeutic implications of anti-PLT agents in future IBD remedies.World Journal of Gastroenterology 03/2014; 20(12):3180-3190. · 2.55 Impact Factor