Maribel Diaz-Ricart

Hospital Clínic de Barcelona, Barcino, Catalonia, Spain

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Publications (146)596.84 Total impact

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    ABSTRACT: Defibrotide (DF) has received EMA authorization to treat sinusoidal obstruction syndrome, an early complication after hematopoietic cell transplantation. DF has a recognized role as an endothelial protective agent, although its precise mechanism of action remains to be elucidated. The aim of the present study was to investigate the interaction of DF with endothelial cells (ECs). A human hepatic endothelial cell line was exposed to different DF concentrations, previously labelled. Using inhibitory assays and flow cytometry techniques along with confocal microscopy, we explored: DF-EC interaction, endocytic pathways, and internalization kinetics. Moreover, we evaluated the potential role of adenosine receptors in DF-EC interaction and if DF effects on endothelium were dependent of its internalization. Confocal microscopy showed interaction of DF with EC membranes followed by internalization, though DF did not reach cell nucleus even after 24h. Flow cytometry revealed concentration, temperature and time dependent up-take of DF in two EC models but not in other cell types. Moreover, inhibitory assays indicated that entrance of DF into ECs occurs primarily through macropinocytosis. Our experimental approach did not show any evidence of the involvement of adenosine receptors in DF-EC interaction. The anti-inflammatory and antioxidant properties of DF seem to be due to the interaction of the drug with the cell membrane. Our findings contribute to a better understanding of the precise mechanisms of action of DF as a therapeutic and potential preventive agent on the endothelial damage underlying different pathological situations.
    No preview · Article · Jan 2016 · Blood
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    ABSTRACT: Background: Cryopreserved platelet (CPP) concentrates exhibit a variety of morphologic and functional alterations that may affect the action of CPP with accelerated platelet (PLT) response and clotting. The objective of this study was to compare the in vitro hemostatic effect of CPP with fresh whole blood (WB) and standard 5-day PLT concentrates (PCs). Study design and methods: WB collected from eight healthy donors was used to prepare fresh WB, PLT-depleted WB (TPN), and PLT-restored TPN using CPP (TPN-CPP) or PC (TPN-PC). Clot properties were evaluated with thromboelastometry (ROTEM); adhesion and aggregate formation under high shear (Impact-R); and PLT adhesion, aggregate formation, fibrin formation, and prothrombin activation under medium shear in a perfusion system. Results: TPN-CPP had faster clot initiation (ROTEM clot time-TPN-CPP 115 sec, WB 194 sec, TPN-PC 161 sec), and CPP contributes to a strong clot with PLT involvement (maximum clot firmness-TPN-CPP 32 mm, WB 62 mm, TPN-PC 59 mm). The Impact-R PLT-covered area with TPN-CPP was less than those of WB and PCs, but aggregate size was the same as WB. PLT coverage in perfusion studies was observed with TPN-CPP, although generally less than both WB and PC. Fibrin was deposited with CPP-restored samples, but did not exceed the level of WB. Conclusion: CPPs present a phenotype supporting a moderate increase in the rate of clot formation, form stable PLT clots, and do not present a hypercoagulable phenotype during in vitro functional tests.
    No preview · Article · Oct 2015 · Transfusion
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    S Fernández · P Castro · P Molina · M Palomo · J Aibar · M Díaz-Ricart · JM Nicolás

    Preview · Article · Oct 2015
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    ABSTRACT: We evaluated the hemostatic alterations in blood from healthy individuals treated for 5 days with direct oral anticoagulants (DOACs) rivaroxaban (20 mg/d) or dabigatran (150 mg/12 h) in a single-blind clinical trial with crossover assignment (NCT01478282). We assessed the potential of prothrombin complex concentrates, activated prothrombin complex concentrates, or recombinant activated factor VII, when added ex vivo, to reverse the alterations caused by these DOACs. Blood was drawn at maximum plasma concentration after the last dose of each DOAC, and modifications in coagulation biomarkers were evaluated using a series of tests performed under steady conditions including routine coagulation, thrombin generation, and thromboelastometry assays. Additional studies in standardized flow devices were applied to evaluate alterations on platelet deposition and fibrin formation on damaged vascular surfaces exposed to flowing blood. Both DOACs caused important modifications of all coagulation biomarkers and significantly reduced fibrin formation in flow studies. Alterations in biomarkers observed in steady laboratory tests were normalized and occasionally overcompensated by procoagulant strategies. In contrast, reductions in fibrin formation observed in studies with flowing blood were improved, although never completely restored to baseline levels. Effects of dabigatran in flow studies appeared more resistant to reversal strategies than those of rivaroxaban. Inconsistencies between results of coagulation studies in steady or flowing assays not only raise concerns about the adequacy of the earlier tests to predict the restoration of the coagulopathy induced by DOACs but also suggest limitations of nonspecific procoagulant strategies to control severe coagulopathy in patients inadvertently overexposed these agents.
    No preview · Article · Sep 2015 · Transfusion medicine reviews
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    ABSTRACT: Platelets are important in hemostasis, but also detect particles and pathogens in the circulation. Phagocytic and endocytic activities of platelets are widely recognized, however, receptors and mechanisms involved remain poorly understood. We previously demonstrated that platelets internalize and store phospholipid microvesicles enriched in human tissue factor (TF + MVs) and that platelet-associated TF enhances thrombus formation at sites of vascular damage. Here we investigate the mechanisms implied in the interactions of TF + MVs with platelets and the effects of specific inhibitory strategies. Aggregometry and electron microscopy were used to assess platelet activation and TF + MVs uptake. Cytoskeletal assembly and activation of phosphoinositide 3-kinase (PI3K) and RhoA were analyzed by western blot and ELISA. Exposure of platelets to TF + MVs caused reversible platelet aggregation, actin polymerization and association of contractile proteins to the cytoskeleton being maximal at 1 min. The same kinetics were observed for activation of PI3K and translocation of RhoA to the cytoskeleton. Inhibitory strategies to block glycoprotein IIb-IIIa (GPIIb-IIIa), scavenger receptor CD36, serotonin transporter (SERT) and PI3K, fully prevented platelet aggregation by TF + MVs. Ultrastructural techniques revealed that uptake of TF + MVs was efficiently prevented by anti-CD36 and SERT inhibitor, but only moderately interfered by GPIIb-IIIa blockade. We conclude that internalization of TF + MVs by platelets occurs independently of receptors related to their main hemostatic function (GPIIb-IIIa), involves the scavenger receptor CD36, SERT and engages PI3-Kinase activation and cytoskeletal assembly. CD36 and SERT appear as potential therapeutic targets to interfere with the association of TF + MVs with platelets and possibly downregulate their prothrombotic phenotype. This article is protected by copyright. All rights reserved
    No preview · Article · Jul 2015 · Journal of Cellular Biochemistry
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    ABSTRACT: Reliable, non-invasive methods for diagnosing and prognosing sinusoidal obstruction syndrome (SOS) early after hematopoietic cell transplantation (HCT) are needed. We used a quantitative mass spectrometry-based proteomics approach to identify candidate biomarkers of SOS by comparing plasma pooled from 20 patients with and 20 patients without SOS. Of 494 proteins quantified, we selected six proteins [L-Ficolin, vascular-cell-adhesion-molecule-1 (VCAM1), tissue-inhibitor of metalloproteinase-1, von Willebrand factor, intercellular-adhesion-molecule-1, and CD97] based on a differential heavy/light isotope ratio of at least 2 fold, information from the literature, and immunoassay availability. Next, we evaluated the diagnostic potential of these six proteins and five selected from the literature [suppression of tumorigenicity-2 (ST2), angiopoietin-2 (ANG2), hyaluronic acid (HA), thrombomodulin, and plasminogen activator inhibitor-1] in samples from 80 patients. The results demonstrate that together ST2, ANG2, L-Ficolin, HA, and VCAM1 compose a biomarker panel for diagnosis of SOS. L-Ficolin, HA, and VCAM1 also stratified patients at risk for SOS as early as the day of HCT. Prognostic Bayesian modeling for SOS onset based on L-Ficolin, HA, and VCAM1 levels on the day of HCT and clinical characteristics showed >80% correct prognosis of SOS onset. These biomarkers may provide opportunities for preemptive intervention to minimize SOS incidence and/or severity. Copyright © 2015 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
    No preview · Article · Jul 2015 · Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation
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    Full-text · Conference Paper · Jun 2015

  • No preview · Conference Paper · May 2015
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    ABSTRACT: Platelet inhibition is a key strategy in the management of atherothrombosis. However, the large variability in response to current strategies leads to the search for alternative inhibitors. The antiplatelet effect of the inorganic salt sodium tungstate (Na2O4W), a protein tyrosine phosphatase 1B (PTP1B) inhibitor, has been investigated in this study. Wild-type (WT) and PTP1B knockout (PTP1B(-/-)) mice were treated for 1 week with Na2O4W to study platelet function with the platelet function analyzer PFA-100, a cone-and-plate analyzer, a flat perfusion chamber, and thrombus formation in vivo. Human blood aliquots were incubated with Na2O4W for 1 hour to measure platelet function using the PFA-100 and the annular perfusion chamber. Aggregometry and thromboelastometry were also performed. In WT mice, Na2O4W treatment prolonged closure times in the PFA-100 and decreased the surface covered (%SC) by platelets on collagen. Thrombi formed in a thrombosis mice model were smaller in animals treated with Na2O4W (4.6±0.7 mg vs 8.9±0.7 mg; P<0.001). Results with Na2O4W were similar to those in untreated PTP1B(-)/(-) mice (5.0±0.3 mg). Treatment of the PTP1B(-)/(-) mice with Na2O4W modified only slightly this response. In human blood, a dose-dependent effect was observed. At 200 μM, closure times in the PFA-100 were prolonged. On denuded vessels, %SC and thrombi formation (%T) decreased with Na2O4W. Neither the aggregating response nor the viscoelastic clot properties were affected. Na2O4W decreases consistently the hemostatic capacity of platelets, inhibiting their adhesive and cohesive properties under flow conditions in mice and in human blood, resulting in smaller thrombi. Although Na2O4W may be acting on platelet PTP1B, other potential targets should not be disregarded.
    Full-text · Article · May 2015 · Drug Design, Development and Therapy
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    ABSTRACT: Severe deficiency of ADAMTS13 activity leads to von Willebrand factor (VWF) ultralarge multimers with high affinity for platelets, causing thrombotic thrombocytopenic purpura. Other pathological conditions with moderate ADAMTS13 activity exhibit a thrombotic risk. We examined the ADAMTS13 activity in systemic lupus erythematosus (SLE) and its value as a thrombotic biomarker. ADAMTS13 activity, VWF antigen and multimeric structure, and vascular cell adhesion molecule 1 (VCAM-1) were measured in plasma samples from 50 SLE patients and 50 healthy donors. Disease activity (systemic lupus erythematosus disease activity index; SLEDAI) and organ damage (systemic lupus international collaborating clinics) scores, thrombotic events, antiphospholipid syndrome (APS) and antiphospholipid antibodies (aPLs) were registered. SLE patients showed decreased ADAMTS13 activity and high VWF levels compared with controls (66 ± 27% vs. 101 ± 8%, P < 0.01, and 325 ± 151% vs. 81 ± 14%, P < 0.001). VCAM-1 levels were higher in SLE patients (P < 0.05). Considering three groups of SLE patients depending on ADAMTS13 activity (>60%, 60-40% and <40%), comparative analysis showed significant association between ADAMTS13 activity and SLEDAI (P < 0.05), presence of aPLs (P < 0.001), APS (P < 0.01) and thrombotic events (P < 0.01). Reduced ADAMTS13 activity together with increased VWF levels were especially notable in patients with active disease and with aPLs. ADAMTS13 activity, in combination with other laboratory parameters, could constitute a potential prognostic biomarker of thrombotic risk in SLE. © The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
    No preview · Article · Mar 2015 · Lupus
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    ABSTRACT: The mobilization pattern and functionality of endothelial progenitor cells after an acute ischemic event remain largely unknown. The aim of our study was to characterize and compare the short-and long-term mobilization of endothelial progenitor cells and circulating endothelial cells after acute myocardial infarction or atherothrombotic stroke, and to determine the relationship between these cell counts and plasma concentrations of vascular cell adhesion molecule (VCAM-1) and Von Willebrand factor (VWF) as surrogate markers of endothelial damage and inflammation. In addi-tion, we assessed whether endothelial progenitor cells behave like functional endothelial cells. We included 150 pa-tients with acute myocardial infarction or atherothrombotic stroke and 145 controls. Endothelial progenitor cells [CD45−, CD34+, KDR+, CD133+], circulating endothelial cells [CD45−, CD146+, CD31+], VWF, and VCAM-1 levels were measured in controls (baseline only) and in patients within 24 h (baseline) and at 7, 30, and 180 days after the event. Myocardial infarction patients had higher counts of endothelial progenitor cells and circulating endo-thelial cells than the controls (201.0/mL vs. 57.0/mL; p b 0.01 and 181.0/mL vs. 62.0/mL; p b 0.01). Endothelial progen-itor cells peaked at 30 days post-infarction (201.0/mL vs. 369.5/mL; p b 0.01), as did VCAM-1 (573.7 ng/mL vs. 701.8 ng/mL; p b 0.01). At 180 days post-infarction, circulating endothelial cells and VWF decreased, compared to base-line. In stroke patients, the number of endothelial progenitor cells — but not circulating endothelial cells — was higher than in controls (90.0/mL vs. 37.0/mL; p = 0.01; 105.0/mL vs. 71.0/mL; p = 0.11). At 30 days after stroke, however, VCAM-1 peaked (628.1/mL vs. 869.1/mL; p b 0.01) but there was no significant change in endothelial progenitor cells (90/mL vs. 78/mL; p b 0.34). At 180 days after stroke, circulating endothelial cells and VWF decreased, compared to baseline. Cultured endothelial progenitor cells from controls and myocardial infarction patients had endothelial phe-notype characteristics and exhibited functional differences in adhesion and Ca 2+ influx, but not in proliferation and vasculogenesis. In myocardial infarction patients, VCAM-1 levels and mobilization of endothelial progenitor cells peaked at 30 days after the ischemic event. Although a similar VCAM-1 kinetic was observed in stroke patients, endo-thelial progenitor cells did not increase. Endothelial progenitor cells had mature endothelial capabilities in vitro.
    Full-text · Article · Jan 2015 · Journal of Molecular and Cellular Cardiology
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    ABSTRACT: Background: Despite the good safety of rivaroxaban, there is limited information on strategies for urgent reversal of its antihemostatic effects. Methods and results: Alterations of hemostasis induced by rivaroxaban (230 ng/ml) were assessed by using several tests applied to steady and circulating human blood. Effects on thrombin generation (TG) and thromboelastometry (TEM) parameters were measured. Modifications in platelet adhesive, aggregating and procoagulant activities were evaluated in studies with circulating blood. The potential reversal of prothrombin complex concentrates (PCCs; 50 IU/kg), activated PCCs (aPCCs; 75 IU/kg), or recombinant factor VIIa (rFVIIa; 270 μg/kg) was evaluated. Impairment of TG parameters induced by rivaroxaban were corrected by the different concentrates (aPCC≥PCC>rFVIIa). Prolonged clotting times and reduced clot firmness caused by rivaroxaban on TEM tests were improved by different concentrates (rFVIIa≥aPCC>PCC). Rivaroxaban significantly reduced platelets and fibrin interactions with damaged vascular surfaces in perfusion studies. While alterations of platelet interactions were favourably counteracted by rFVIIa or aPCCs, reductions in fibrin formation were only partially restored by the different factor concentrates (rFVIIa>aPCC≥PCC). Conclusions: Rivaroxaban-induced alterations on coagulation parameters measured through assays performed under static conditions were easily reversed by the different concentrates. Studies under flow conditions revealed that these concentrates normalized the action of rivaroxaban on platelets, and significantly improved fibrin formation; although in the later case, levels were not restored to the pre-treatment value.
    Full-text · Article · Dec 2014 · Circulation Journal
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    ABSTRACT: Thrombotic microangiopathies (TMA) are disorders defined by the presence of a microangiopathic hemolytic anemia (with the characteristic hallmark of schistocytes in the peripheral blood smear), thrombocytopenia and organ malfunction of variable intensity. Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are the most important forms of TMA and, without the adequate treatment, they are associated with high morbimortality. In recent years, significant advances in the knowledge of the pathophysiology of TMA have occurred. Those advances have allowed us to move from a syndromic diagnosis with a similar treatment to all entities to the search of etiologic diagnosis which would lead to a specific treatment, finally leading to a better outcome of the patient. This document pretends to summarize the current status of knowledge of the pathophysiology of TMA and the therapeutic options available, and to offer a diagnostic and therapeutic practical tool to the professionals caring for the patients. Copyright © 2014 Elsevier España, S.L.U. All rights reserved.
    Full-text · Article · Nov 2014 · Medicina Clínica
  • M Diaz-Ricart · G Escolar
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    ABSTRACT: Vorapaxar is a novel platelet inhibitor that potently and selectively inhibits thrombin-mediated platelet activation without interfering with thrombin-mediated cleavage of fibrinogen via antagonism of the platelet proteinase-activated receptor PAR1. Vorapaxar is a non-peptide himbacine analogue that has been developed for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction or peripheral arterial disease. Copyright 2014 Prous Science, S.A.U. or its licensors. All rights reserved.
    No preview · Article · Nov 2014 · Drugs of today (Barcelona, Spain: 1998)

  • No preview · Article · Oct 2014 · International Journal of Cardiology

  • No preview · Article · May 2014 · Thrombosis Research
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    ABSTRACT: Background Serotonergic mechanisms have been suggested as a link between major depression and cardiovascular risk. We investigated the existence of a prothrombotic condition in depressed patients and its possible modulation during treatment with a selective serotonin-reuptake inhibitor (SSRI). Methods Modifications in a series of biomarkers of platelet and coagulation activation were evaluated in blood from 19 patients with a major depression disorder (MDD) at the time of diagnosis, and at 8 and 24 weeks of treatment with escitalopram. Response of blood aliquots recirculated through a thrombogenic surface was assessed in a thrombosis model. Results were compared with those of 20 healthy-matched controls. Results In comparison with controls, platelets from MDD patients showed elevated volumes (p<0.01), significantly enhanced aggregating response to arachidonic acid and augmented expression of GPIb, fibrinogen, factor V, and anionic phospholipids by flow cytometry (p<0.05). Clot firmness and procoagulant activity of platelet-associated tissue factor were also significantly elevated (p<0.05). Studies with circulating blood revealed increased fibrin formation in early diagnosed patients (71.1±9.5% vs. 45.8±5.3%; p<0.05 vs. controls). After 24 weeks of treatment with escitalopram, the majority of the alterations observed were normalized, except for a residual increased expression of GPIIbIIIa (p<0.05) and persistent alterations in thromboelatometic parameters. Limitations Despite the reduced number of followed-up patients our findings were consistent reaching statistical significance. Conclusions Our results reveal a prothrombotic phenotype in MDD patients. While continuous treatment with an SSRI downregulated the majority of the biomarkers analyzed, alterations in viscoelastic parameters of clot formation remained unaffected by the antidepressant treatment.
    No preview · Article · Apr 2014 · Journal of Affective Disorders
  • Gines Escolar · Maribel Diaz-Ricart · Eduardo Arellano-Rodrigo · Ana M Galán
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    ABSTRACT: Introduction: Thromboembolic diseases will become the most important contributors to mortality and morbidity for modern societies. Current antithrombotic strategies using heparins or vitamin K antagonists are inconvenient, with limitations and inherent side effects. A series of new oral anticoagulants with powerful and reliable antithrombotic actions have been developed in the last decade. Areas covered: Edoxaban is a direct and specific inhibitor of activated factor X, delivered orally. This article reviews literature from PubMed and articles referenced within. The text explores the pharmacological aspects of its antithrombotic action. Pharmacokinetics, metabolism and drug interactions are examined. The review places the results of recent clinical trials that have evaluated the antithrombotic potential of edoxaban versus standard antithrombotic therapies in the prophylaxis and treatment of venous thromboembolism into perspective. The possible relationship between the pharmacokinetic profile of edoxaban and the favorable results in clinical trials is discussed. Expert opinion: Edoxaban is perceived as a major advance, compared to vitamin K antagonists, in the prevention and treatment of thromboembolic disease given its favorable efficacy, safety, pharmacokinetic profile and renal clearance. The results of ongoing large international trials exploring the prevention of thrombotic complications in patients in different clinical settings should ensure the approval of edoxaban to treat new indications.
    No preview · Article · Jan 2014 · Expert Opinion on Drug Metabolism & Toxicology
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    ABSTRACT: Apixaban is a new oral anticoagulant with a specific inhibitory action on FXa. No information is available on the reversal of the antihemostatic action of apixaban in experimental or clinical settings. We have evaluated the effectiveness of different factor concentrates at reversing modifications of hemostatic mechanisms induced by moderately elevated concentrations of apixaban (200 ng/ml) added in vitro to blood from healthy donors (n = 10). Effects on thrombin generation (TG) and thromboelastometry (TEM) parameters were assessed. Modifications in platelet adhesive, aggregating and procoagulant activities were evaluated in studies with blood circulating through damaged vascular surfaces, at a shear rate of 600 s(-1). The potential of prothrombin complex concentrates (PCCs; 50 IU/kg), activated prothrombin complex concentrates (aPCCs; 75 IU/kg), or activated recombinant factor VII (rFVIIa; 270 μg/kg), at reversing the antihemostatic actions of apixaban, were investigated. Apixaban interfered with TG kinetics. Delayed lag phase, prolonged time to peak and reduced peak values, were improved by the different concentrates, though modifications in TG patterns were diversely affected depending on the activating reagents. Apixaban significantly prolonged clotting times (CTs) in TEM studies. Prolongations in CTs were corrected by the different concentrates with variable efficacies (rFVIIa≥aPCC>PCC). Apixaban significantly reduced fibrin and platelet interactions with damaged vascular surfaces in perfusion studies (p<0.05 and p<0.01, respectively). Impairments in fibrin formation were normalized by the different concentrates. Only rFVIIa significantly restored levels of platelet deposition. Alterations in hemostasis induced by apixaban were variably compensated by the different factor concentrates investigated. However, effects of these concentrates were not homogeneous in all the tests, with PCCs showing more efficacy in TG, and rFVIIa being more effective on TEM and perfusion studies. Our results indicate that rFVIIa, PCCs and aPCCs have the potential to restore platelet and fibrin components of the hemostasis previously altered by apixaban.
    Full-text · Article · Nov 2013 · PLoS ONE
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    ABSTRACT: Endothelial dysfunction seems to be a key factor in the development of several complications observed early after hematopoietic stem cell transplantation (HSCT). The conditioning regimen and many other factors associated with the procedure are responsible for this endothelial damage. The effects of immunosuppressive agents on endothelial function have not been explored in detail. We evaluated the effects of three of the drugs commonly used in HSCT: two calcineurin inhibitors, cyclosporine A (CSA) and tacrolimus (TAC), and an inhibitor of mTOR, sirolimus (SIR). We also evaluated the effect of the combination of TAC and SIR (TAC+SIR), which is used increasingly in clinical practice. Microvascular endothelial cells (HMEC-1) were exposed to these drugs to evaluate changes in: i) ICAM-1 expression on the cell surface, assessed by immunofluorescence labeling and expressed as the mean gray value (MGV); ii) reactivity of the extracellular matrix (ECM) toward platelets, upon exposure of the ECM to circulating blood; and iii) whole-blood clot formation, assessed by thromboelastometry. Studies were conducted in the absence and presence of defibrotide (DF) to assess its possible protective effect. The exposure of HMEC-1 to CSA and TAC+SIR significantly increased the expression of ICAM-1 (157.5±11.6 and 153.4±9.5 MGV, respectively, vs. 105.7±6.5 MGV in controls (both P<0.05)). TAC applied alone increased ICAM-1 slightly (120.3±8.2 MGV), and SIR had no effect (108.9±7.4 MGV). ECM reactivity increased significantly only in response to CSA (surface covered by platelets of 41.2%±5.4% vs. 30.1%±2.0%, P<0.05). DF attenuated all of these changes. No significant changes in the viscoelastic properties of clot formation were observed in any condition with blood samples incubated in vitro. In conclusion, CSA and TAC+SIR had a proinflammatory effect, but only CSA exhibited an additional prothrombotic effect. Interestingly, DF exerted clear protective anti-inflammatory and antithrombotic effects on the endothelium.
    Preview · Article · Jul 2013 · Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation

Publication Stats

1k Citations
596.84 Total Impact Points

Institutions

  • 1992-2016
    • Hospital Clínic de Barcelona
      • • Centro de Diagnóstico Biomédico, CDB
      • • Servicio de Hemoterapia y Hemostasia
      Barcino, Catalonia, Spain
  • 2009-2015
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 1990-2015
    • University of Barcelona
      • • Department of Medicine
      • • Facultad de Medicina
      Barcino, Catalonia, Spain
  • 2000-2011
    • IDIBAPS August Pi i Sunyer Biomedical Research Institute
      Barcino, Catalonia, Spain
  • 2008
    • Southern Medical Clinic
      San Fernando, City of San Fernando, Trinidad and Tobago
  • 1996-2006
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
    • Medical University of South Carolina
      Charleston, South Carolina, United States
  • 1996-1998
    • Kurume University
      • Division of Protein Biochemistry
      Куруме, Fukuoka, Japan