References of "Oury, Cécile"
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See detailImpact of Serial B-Type Natriuretic Peptide Changes for Predicting Outcome in Asymptomatic Patients With Aortic Stenosis.
Henri, Christine; DULGHERU, Raluca Elena ULg; Magne, Julien et al

in The Canadian journal of cardiology (2015)

BACKGROUND: The aim of this study was to determine the impact on the outcome of serial B-type natriuretic peptide (BNP) changes during follow-up in asymptomatic patients with >/= moderate aortic stenosis ... [more ▼]

BACKGROUND: The aim of this study was to determine the impact on the outcome of serial B-type natriuretic peptide (BNP) changes during follow-up in asymptomatic patients with >/= moderate aortic stenosis (AS) and preserved left ventricular ejection fraction. METHODS: We prospectively screened 69 patients who underwent comprehensive transthoracic echocardiography, BNP level measurement at baseline and after every 6 or 12 months. Annualized BNP changes were calculated as the difference between the last and baseline BNP measurements divided by the duration of follow-up. The primary endpoint was the occurrence of symptoms, aortic valve replacement, or cardiovascular death. RESULTS: During a follow-up of 30 +/- 19 months, 43 patients experienced a cardiac event. These patients were significantly older (73 +/- 9 vs 65 +/- 16 years; P = 0.010), had more often dyslipidemia (79% vs 42%; P = 0.038), more severe AS (peak velocity: 3.9 +/- 0.6 vs 3.5 +/- 0.6 m/s; P = 0.002), larger indexed left atrial area (10.2 +/- 2.5 vs 8.7 +/- 1.9 cm2/m2; P = 0.006), and a higher increase in annualized BNP (+90 +/- 155 vs +7 +/- 49 pg/mL/y; P = 0.010). Patients with higher annualized BNP changes (> 20 pg/mL/y) had a significantly lower cardiac event-free survival (1 year: 63 +/- 8% vs 97 +/- 3%; 3 years: 31 +/- 8% vs 68 +/- 8%; P < 0.001). Using the multivariate Cox proportional hazards model, higher annualized BNP changes were significantly associated with increased risk of cardiac events (hazard ratio: 2.73, 95% confidence interval: 1.27-5.86; P = 0.010) after adjustment for age, dyslipidemia, and echocardiographic parameters. CONCLUSIONS: In asymptomatic patients with AS and preserved left ventricular ejection fraction, the use of serial BNP changes may help to anticipate development of class I indication for aortic valve replacement. [less ▲]

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See detailErratum: Elevated basal levels of circulating activated platelets predict ICU-acquired sepsis and mortality: a prospective study.
Layios, N.; Delierneux, Céline ULg; Hego, A. et al

in Critical care (London, England) (2015), 19(1), 301

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See detailErratum: Prospective immune profiling in critically ill adults: before, during and after severe sepsis and septic shock.
Layios, N.; GOSSET, Christian ULg; Delierneux, Céline ULg et al

in Critical care (London, England) (2015), 19(1), 300

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See detailPositron Emission Tomography/Computed Tomography Imaging in Device Infective Endocarditis: Ready for Prime Time
Lancellotti, Patrizio ULg; Habib, Gilbert; Oury, Cécile ULg et al

in Circulation (2015)

Over the last decade there has been a remarkable increase in prosthetic heart valve replacement and cardiac implantable electronic device utilization. Although capable of improving the quality and ... [more ▼]

Over the last decade there has been a remarkable increase in prosthetic heart valve replacement and cardiac implantable electronic device utilization. Although capable of improving the quality and quantity of life of patients suffering from severe valvular heart disease or rhythm disorders, they are both subject to potentially life-threatening infection involving the endocardium, referred to as device infective endocarditis (DIE)1,2. The rate of prosthetic valve endocarditis (PVE) ranges from 1-6% to 15%, being higher in revision surgery1. The infection usually involves the junction between the sewing ring and the annulus, leading to perivalvular abscess, dehiscence, pseudo-aneurysms, and fistulae, or the leaflets of the prosthesis, leading to vegetations, cusp rupture, and perforation. Cardiac device-related infective endocarditis (CDRIE), to be distinguished from local device infection (pocket/generator), is defined as an infection involving the electrode leads, cardiac valve leaflets, or endocardial surface. An incidence of 1.4 per 1000 device-years of definite CDRIE has been reported3. DIE may occur at anytime, being related to surgery only in early cases. [less ▲]

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See detailLes antiplaquettaires : quoi de neuf ?
Oury, Cécile ULg; Rahmouni, Souad ULg; LANCELLOTTI, Patrizio ULg

in Medecine Sciences : M/S (2015)

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See detailLeft ventricular regional function and maximal exercise capacity in aortic stenosis.
DULGHERU, Raluca Elena ULg; Magne, J.; DAVIN, Laurent ULg et al

in European heart journal cardiovascular Imaging (2015)

AIMS: The objective assessment of maximal exercise capacity (MEC) using peak oxygen consumption (VO2) measurement may be helpful in the management of asymptomatic aortic stenosis (AS) patients. However ... [more ▼]

AIMS: The objective assessment of maximal exercise capacity (MEC) using peak oxygen consumption (VO2) measurement may be helpful in the management of asymptomatic aortic stenosis (AS) patients. However, the relationship between left ventricular (LV) function and MEC has been relatively unexplored. We aimed to identify which echocardiographic parameters of LV systolic function can predict MEC in asymptomatic AS. METHODS AND RESULTS: Asymptomatic patients with moderate to severe AS (n = 44, aortic valve area <1.5 cm2, 66 +/- 13 years, 75% of men) and preserved LV ejection fraction (LVEF > 50%) were prospectively referred for resting echocardiography and cardiopulmonary exercise test. LV longitudinal strain (LS) of each myocardial segment was measured by speckle tracking echocardiography (STE) from the apical (aLS) 4-, 2-, and 3-chamber views. An average value of the LS of the analysable segments was provided for each myocardial region: basal (bLS), mid (mLS), and aLS. LV circumferential and radial strains were measured from short-axis views. Peak VO2 was 20.1 +/- 5.8 mL/kg/min (median 20.7 mL/kg/min; range 7.2-32.3 mL/kg/min). According to the median of peak VO2, patients with reduced MEC were significantly older (P < 0.001) and more frequently females (P = 0.05). There were significant correlations between peak VO2 and age (r = -0.44), LV end-diastolic volume (r = 0.35), LV stroke volume (r = 0.37), indexed stroke volume (r = 0.32), and E/e' ratio (r = -0.37, all P < 0.04). Parameters of AS severity and LVEF did not correlate with peak VO2 (P = NS for all). Among LV deformation parameters, bLS and mLS were significantly associated with peakVO2 (r = 0.43, P = 0.005, and r = 0.32, P = 0.04, respectively). With multivariable analysis, female gender (beta = 4.9; P = 0.008) and bLS (beta = 0.50; P = 0.03) were the only independent determinants (r2 = 0.423) of peak VO2. CONCLUSION: In asymptomatic AS, impaired LV myocardial longitudinal function determines reduced MEC. Basal LS was the only parameter of LV regional function independently associated with MEC. [less ▲]

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See detailPoster session 6: Saturday 6 December 2014, 08:30-12:30Location: Poster area.
Henri, C.; DULGHERU, Raluca Elena ULg; Magne, J. et al

Poster (2014, December)

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See detailPoster session 5: Friday 5 December 2014, 14:00-18:00Location: Poster area.
Henri, C.; DULGHERU, Raluca Elena ULg; Magne, J. et al

Poster (2014, December)

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See detailP2X1 expressed on polymorphonuclear neutrophils and platelets is required for thrombosis in mice
Darbousset, Roxane; Delierneux, Céline ULg; Mezouar, Soraya et al

in Blood (2014), 124

Adenosine Triphosphate (ATP) and its metabolite, adenosine, are key regulators of polymorphonuclear neutrophils (PMNs) functions. PMNs have recently been implicated in the initiation of thrombosis. We ... [more ▼]

Adenosine Triphosphate (ATP) and its metabolite, adenosine, are key regulators of polymorphonuclear neutrophils (PMNs) functions. PMNs have recently been implicated in the initiation of thrombosis. We investigated the role of ATP and adenosine in PMN activation and recruitment at the site of endothelial injury. Following binding to the injured vessel wall, PMNs are activated and release elastase. The recruitment of PMNs and the subsequent fibrin generation and thrombus formation are strongly affected in mice deficient in the P2X1-ATP receptor and in wild-type mice treated with CGS 21680, an agonist of the A2A adenosine receptor or NF449 a P2X1 antagonist. Infusion of wild-type PMNs into P2X1-deficient mice increases fibrin generation but not thrombus formation. Restoration of thrombosis requires infusion of both platelets and PMNs from wild-type mice. In vitro, ATP activates PMNs, whereas CGS 21680 prevents their binding to activated endothelial cells. These data indicate that ATP contributes to PMN activation leading to their adhesion at the site of laser-induced endothelial injury, a necessary step leading to the generation of fibrin and subsequent platelet-dependent thrombus formation. Altogether, our study identifies previously unknown mechanisms by which ATP and adenosine are key molecules involved in thrombosis by regulating the activation state of PMNs. [less ▲]

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See detailRasa3 Controls Megakaryocyte Rap1 Activation, Integrin Signaling and Differentiation into Proplatelet
Molina Ortiz, Patricia ULg; Polizzi, Séléna; Ramery, Eve ULg et al

in PLoS Genetics (2014), 10(6), 1004420

Rasa3 is a GTPase activating protein of the GAP1 family which targets Ras and Rap1. Ubiquitous Rasa3 catalytic inactivation in mouse results in early embryonic lethality. Here, we show that Rasa3 ... [more ▼]

Rasa3 is a GTPase activating protein of the GAP1 family which targets Ras and Rap1. Ubiquitous Rasa3 catalytic inactivation in mouse results in early embryonic lethality. Here, we show that Rasa3 catalytic inactivation in mouse hematopoietic cells results in a lethal syndrome characterized by severe defects during megakaryopoiesis, thrombocytopenia and a predisposition to develop preleukemia. The main objective of this study was to define the cellular and the molecular mechanisms of terminal megakaryopoiesis alterations. We found that Rasa3 catalytic inactivation altered megakaryocyte development, adherence, migration, actin cytoskeleton organization and differentiation into proplatelet forming megakaryocytes. These megakaryocyte alterations were associated with an increased active Rap1 level and a constitutive integrin activation. Thus, these mice presented a severe thrombocytopenia, bleeding and anemia associated with an increased percentage of megakaryocytes in the bone marrow, bone marrow fibrosis, extramedular hematopoiesis, splenomegaly and premature death. Altogether, our results indicate that Rasa3 catalytic activity controls Rap1 activation and integrin signaling during megakaryocyte differentiation in mouse. [less ▲]

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See detailCAMKKβ/AMPK-α1 pathway regulates phosphorylation of cytoskeletal targets in thrombin-stimulated human platelets
Onselaer, Marie-Blanche; Oury, Cécile ULg; Hunter, Roger W et al

in Journal of Thrombosis and Haemostasis [=JTH] (2014), 12(6), 973-986

Background. Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In various other cell types, AMP-activated protein kinase ... [more ▼]

Background. Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In various other cell types, AMP-activated protein kinase (AMPK) controls the phosphorylation state of cytoskeletal targets. Objective. We hypothesized that AMPK is activated during platelet aggregation and contributes to the control of cytoskeletal targets. Results. We found that AMPK-α1 was mainly activated by thrombin and not by other platelet agonists in purified human platelets. Thrombin activated AMPK-α1 ex vivo via a Ca2+/calmodulin-dependent kinase kinase β (CAMKKβ)-dependent pathway. Pharmacological inhibition of CAMKKβ blocked thrombin-induced platelet aggregation and counteracted thrombin-induced phosphorylation of several cytoskeletal proteins, namely, regulatory myosin light chains (MLC), cofilin and vasodilator-stimulated phosphoprotein (VASP), three key elements involved in actin cytoskeleton contraction and polymerization. Platelets isolated from mice lacking AMPK-α1 exhibited reduced aggregation in response to thrombin, associated with a defect in MLC, cofilin and VASP phosphorylation and actin polymerization. More importantly, we show for the first time that AMPK pathway was activated in platelets of patients undergoing major cardiac surgery, in a heparin-sensitive manner. Conclusion. AMPK-α1 is activated by thrombin in human platelets. It controls phosphorylation of key cytoskeletal targets and actin cytoskeleton remodelling during platelet aggregation. [less ▲]

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See detailCombined use of GWAS and eQTL information to identify genes controlling platelet biology
Gori, Ann-Stephan ULg; LECUT, Christelle ULg; Theatre, Emilie ULg et al

Poster (2014, April 24)

Genome Wide Association Studies (GWAS) have identified at least 68 loci involved in megakaryopoiesis and platelet formation. As for all GWAS, identified risk loci span hundreds of kilobases encompassing ... [more ▼]

Genome Wide Association Studies (GWAS) have identified at least 68 loci involved in megakaryopoiesis and platelet formation. As for all GWAS, identified risk loci span hundreds of kilobases encompassing multiple genes, such that causative variants and genes remain largely unknown. To aid in the identification of causative genes underlying GWAS hits for platelet function (as well as other phenotypes including common complex diseases), we have generated a dataset (" CEDAR ") comprising genome-wide SNP and transcriptome data on nine primary cell types, including platelets, for 330 healthy Caucasian individuals. In addition, we have measured platelet counts and volume, as well as platelet reactivity to ADP, collagen and thrombin-related peptide for all these individuals. After extensive quality control, the ensuing data set has been used to identify (i) QTL influencing platelet count, volume and reactivity, and (ii) cis-and transacting eQTL operating in platelets. To aid in the identification of genes underlying platelet biology, we are applying a recently developed method to search for correlations between association patterns with platelet phenotypes and eQTL association patterns. Such findings would strongly incriminate the corresponding genes (affected by the eQTL) as being causally involved in determining the cognate platelet phenotype. Latest results will be presented. [less ▲]

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See detailUsefulness of Serial B-type Natriuretic Peptide Assessment in Asymptomatic Aortic Stenosis.
Henri; Magne; DULGHERU, Raluca Elena ULg et al

in The American journal of cardiology (2014)

B-type natriuretic peptide (BNP) level may be a useful prognostic marker for the management of asymptomatic patients with aortic stenosis (AS). The aim of this study was to identify the echocardiographic ... [more ▼]

B-type natriuretic peptide (BNP) level may be a useful prognostic marker for the management of asymptomatic patients with aortic stenosis (AS). The aim of this study was to identify the echocardiographic determinants of BNP changes during follow-up in AS. We studied 61 asymptomatic patients with greater than moderate AS and preserved left ventricular (LV) ejection fraction who underwent rest and exercise Doppler echocardiography with concomitant BNP level measurement at baseline. BNP measurement was repeated after inclusion every 6 months. Patients were divided into 2 groups according to the median of BNP changes during follow-up. According to parameters at rest, patients in the high BNP changes group had significantly higher E/e' ratio. Statistically significant correlations were found between BNP changes and E/e' ratio and indexed left atrial area. According to exercise parameters, patients in the high BNP changes group had significantly lower exercise-induced increase in LV ejection fraction. Statistically significant correlations were found between BNP changes and exercise-induced changes in LV ejection fraction. After adjustment for age, mean aortic pressure gradient, and BNP level at baseline, multivariate analysis identified indexed left atrial area, E/e' at rest, and exercise-induced increase in ejection fraction as independent determinants of BNP changes during follow-up. In conclusion, this study shows that, in asymptomatic patients with preserved LV function and moderate AS, serial BNP measurements may widely vary. Subclinical LV diastolic and systolic dysfunctions are frequently present in patients with higher serial BNP changes. [less ▲]

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See detailIdentification of a microRNA landscape targeting the PI3K/Akt signaling pathway in inflammation-induced colorectal carcinogenesis
JOSSE, Claire ULg; Bouznad, Nassim ULg; Geurts, Pierre ULg et al

in American Journal of Physiology - Gastrointestinal and Liver Physiology (2014), 306

Inflammation can contribute to tumor formation; however, markers that predict progression are still lacking. In the present study, the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS ... [more ▼]

Inflammation can contribute to tumor formation; however, markers that predict progression are still lacking. In the present study, the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model of colitis-associated cancer was used to analyze microRNA (miRNA) modulation accompanying inflammation-induced tumor development and to determine whether inflammation-triggered miRNA alterations affect the expression of genes or pathways involved in cancer. A miRNA microarray experiment was performed to establish miRNA expression profiles in mouse colon at early and late time points during inflammation and/or tumor growth. Chronic inflammation and carcinogenesis were associated with distinct changes in miRNA expression. Nevertheless, prediction algorithms of miRNA-mRNA interactions and computational analyses based on ranked miRNA lists consistently identified putative target genes that play essential roles in tumor growth or that belong to key carcinogenesis-related signaling pathways. We identified PI3K/Akt and the insulin growth factor-1 (IGF-1) as major pathways being affected in the AOM/DSS model. DSS-induced chronic inflammation downregulates miR-133a and miR-143/145, which is reportedly associated with human colorectal cancer and PI3K/Akt activation. Accordingly, conditioned medium from inflammatory cells decreases the expression of these miRNA in colorectal adenocarcinoma Caco-2 cells. Overexpression of miR-223, one of the main miRNA showing strong upregulation during AOM/DSS tumor growth, inhibited Akt phosphorylation and IGF-1R expression in these cells. Cell sorting from mouse colons delineated distinct miRNA expression patterns in epithelial and myeloid cells during the periods preceding and spanning tumor growth. Hence, cell-type-specific miRNA dysregulation and subsequent PI3K/Akt activation may be involved in the transition from intestinal inflammation to cancer. [less ▲]

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See detailCD36: linking lipids to the NLRP3 inflammasome, atherogenesis and atherothrombosis
Oury, Cécile ULg

in Cellular & Molecular Immunology (2014), 11

Uptake of the atherogenic lipid mediator oxLDL by CD36 results in the formation of intracellular cholesterol crystals that caused lyso¬somal destabilization and NLRP3 activation. oxLDL not only primes ... [more ▼]

Uptake of the atherogenic lipid mediator oxLDL by CD36 results in the formation of intracellular cholesterol crystals that caused lyso¬somal destabilization and NLRP3 activation. oxLDL not only primes, via a NF-κB-dependent pathway, but also activates NLRP3. CD36-mediated inflammasome activation provides an early pathogenic pathway that links cholesterol accumulation to the chronic inflammatory process of atherosclerosis. During atherogenesis, activated or injured endothelial cells, leucocytes and platelets release ATP that acts in a paracrine manner to transduce sterile inflammatory signals. Among these signals, P2X7 receptors mediate K+ efflux leading to NLRP3 activation. Since ATP assembles ASC complexes in oxLDL-treated macrophages, P2X7 receptors and CD36 may cooperate in vivo to activate NLRP3 inflammasome, contributing to plaque formation. Besides macrophages, CD36 is expressed on platelets where it mediates oxLDL-dependent platelet activation and potentially further IL-1β release. P2X7 receptors contributes to protein disulfide isomerase (PDI) tissue factor-dependent thrombosis. Consequently, both CD36 and P2X7 receptors may be involved in atherothrombosis upon plaque rupture. [less ▲]

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See detailConnection between cardiac vascular permeability, myocardial oedema and inflammation during sepsis: role of the alpha1AMPK isoform
Castanares-Zapatero, Diego; Bouleti, C; Sommereyns, C et al

in Critical Care Medicine (2013), 41(12), 411-22

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence ... [more ▼]

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence vascular permeability and inflammation, thereby counteracting cardiac wall oedema during sepsis. Design: Controlled animal study Settings: University research laboratory Subjects: C57BL/6J, α1AMPK-/- and α1AMPK+/+ mice Intervention: Sepsis was triggered in vivo using a sub-lethal injection of lipopolysaccharide (LPS, O55B5, 10 mg.kg-1), inducing systolic left ventricular (LV) dysfunction. LV function, oedema, vascular permeability and inflammation were assessed in vivo in both wild type (WT) mice (α1AMPK+/+) and α1AMPK-deficient mice (α1AMPK-/-). 5-Aminoimidazole-4-carboxamide riboside (AICAr) served to study the impact of AMPK activation on vascular permeability in vivo. The integrity of EC monolayers was also examined in vitro after LPS challenge in the presence of AICAr and/or after α1AMPK silencing. Measurements and main results: α1AMPK-deficiency dramatically impaired tolerance to LPS challenge. Indeed, α1AMPK-/- exhibited heightened cardiac vascular permeability after LPS challenge compared to α1AMPK+/+. Consequently, an increase in LV mass corresponding to exaggerated wall oedema occurred in α1AMPK-/-, without any further decrease in systolic function. Mechanistically, the LPS-induced α1AMPK-/- cardiac phenotype could not be attributed to major changes in the systemic inflammatory response, but was due to an increased disruption of interendothelial tight junctions. Accordingly, AMPK activation by AICAr counteracted LPS-induced hyperpermeability in WT mice in vivo as well as in ECs in vitro. This effect was associated with a potent protection of ZO-1 linear border pattern in ECs. Conclusions: Our results demonstrate, for the first time the involvement of a signalling pathway in the control of LV wall oedema during sepsis. AMPK exerts a protective action through the preservation of interendothelial tight junctions. Interestingly, exaggerated LV wall oedema was not coupled with aggravated systolic dysfunction. However, it could contribute to diastolic dysfunction in septic patients. [less ▲]

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See detailCompetitive interaction of a synthetic polycation (PDMAEMA) to human platelets and erythrocytes
Flebus, Luca ULg; Lombart, François ULg; martinez, Lucia et al

Poster (2013, October)

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See detailStudy of the specific interaction between fluorescent PDMAEMA and Platelets compared to Erythrocytes
Flebus, Luca ULg; Lombart, François ULg; Martinez, Lucia et al

Poster (2013, June 18)

Nowadays synthetic polymers provide more and more functionalities in the biomedical world, in particular as part of medical devices and drug delivery systems. Looking for new applications in the ... [more ▼]

Nowadays synthetic polymers provide more and more functionalities in the biomedical world, in particular as part of medical devices and drug delivery systems. Looking for new applications in the cardiovascular field, our attention has been focused on the well-known poly(2-(dimethylamino)ethyl methacrylate polymer (PDMAEMA). This synthetic polycation has particularly been studied as a potential DNA carrier to promote cell transfection. However and surprisingly enough relative few studies have been published in order to better understand its hemoreactivity under a free form (thus not based on “PolyElectrolyte Complex”), but also its biodistribution and clearance kinetics. In order to facilitate the in vitro and in vivo monitoring of this polycation and especially to follow its reactivity with whole blood we have labeled it with fluorescein adopting a new chemical route of synthesis. After its thorough purification and full-characterization (NMR, SEC, fluorescent spectroscopy), we followed its interaction with erythrocytes and platelets using flow cytometry. Dose-response curves were established in whole blood and within incubation times ranging between 5 min to 3 h. Considering the largest area and more negative Zeta potential developed by red blood cells compared to platelets, we initially hypothesized that RBC should interact more quickly and efficiently with the polycation. Unexpectedly, platelets presented a higher affinity for the polycation with a saturation binding curve whilst a linear profile was observed for the erythrocyte adsorption curve. Aggregometry analyses also revealed this phenomenon, although displaying a weaker effect in whole blood compared to washed platelets. Ongoing research seeks to understand the molecular mechanism of interaction of this polymer with platelets. [less ▲]

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