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Publications (6)21.59 Total impact

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    ABSTRACT: To assess whether circulating endothelial progenitor cells (CEPCs) can be considered as a cardiovascular risk marker before event has occurred, that is less firmly established than in clinically overt atherosclerosis. Number of CD34+KDR+ cell number per ml blood was measured by flow cytometry in 84 untreated subjects without cardiovascular disease. Atherosclerotic plaque was detected by ultrasound in carotid, abdominal aortic and femoral sites and the number of sites affected by plaque among these three sites was counted as 0, 1, 2 or 3. Additionally, intima-media thickness (IMT) was measured by computerized ultrasound imaging of both common carotid segments. CD34+KDR+ cell number decreased by 48, 29 or 30% in the presence of carotid, aortic or femoral plaque (p<0.001, 0.05, 0.05, respectively) as compared to the absence of plaque and by 70% in the presence of three sites affected with plaque as compared with 0 site with plaque (p<0.01) but did not change with increasing IMT tertiles. Adjustment for Framingham risk score, that was also associated with decreased CD34+KDR+ cell number (p<0.001), made CD34+KDR+ cell number associations with plaque insignificant, except at the carotid site (p<0.01). Reduced CEPC number may participate to preclinical stage of atherosclerosis and provide additional information to traditional risk factors as regards global risk assessment.
    Atherosclerosis 04/2007; 191(1):115-20. · 3.97 Impact Factor
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    ABSTRACT: cGMP regulates vascular smooth muscle tone and arterial wall response to proliferative signals. We determined plasma cGMP and carotid artery intima-media thickness (IMT) and diameter in 84 asymptomatic men submitted to investigation of their cardiovascular risk profiles. Plasma cGMP was positively associated with IMT (P<0.01) and diameter (P<0.05), independently of coexisting risk factors. These associations were reinforced in the subgroup of subjects with high-sensitivity C-reactive protein level or multiple atherosclerotic plaques. A positive relationship existed between diameter and IMT (P<0.01) and disappeared after cGMP adjustment. This suggests a link between cGMP pathway and arterial wall geometry that is revealed by vascular injury conditions and may participate in early large artery remodeling.
    Hypertension 12/2004; 44(6):919-23. · 7.63 Impact Factor
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    ABSTRACT: Intravenous gamma-immunoglobulin (i.v.Ig) is commonly used in the treatment of autoimmune and inflammatory vascular disorders to prevent thrombotic complications. The mechanism of action of i.v.Ig is, however, not yet elucidated. In view of this, we investigated the ability of i.v.Ig to modulate i) Ca(2+) signals of fura-2 loaded endothelial cells, and ii) the associated release of nitric oxide (NO) and von Willebrand factor (vWf). NO was measured either indirectly by radioimmunoassay of cGMP in unstimulated cells or directly by electrochemistry at the surface of stimulated endothelial cells from human umbilical cord veins (HUVEC). Short-term treatment of unstimulated HUVEC with intact i.v.Ig decreased the basal cytosolic Ca(2+) concentration by 20% while it activated the NO/cGMP synthesis. Following i.v.Ig treatment of HUVEC, the Ca(2+) liberation from internal stores and the vWf secretion induced by ATP, thrombin or histamine were significantly reduced by 38 and 60%, respectively. The effects on Ca(2+) signals were observed with intact i.v.Ig as well as with the F(ab')2 or the Fc fragments indicating that both portions are involved in the mechanism of action. The i.v.Ig treatment of HUVECs had no effect on the NO release induced by thrombin or histamine. By contrast, the i.v.Ig treatment increased the ATP-activated NO release by amplifying the Ser1177-eNOS phosphorylation. The i.v.Ig also activated the NO-dependent cGMP release in resting and collagen-stimulated platelets. Since NO is a potent inhibitor of platelet activation and vWF is a platelet adhesion cofactor, the beneficial effects of therapeutic i.v.Ig may lie in the inhibition of platelet adhesion to damaged endothelium.
    Thrombosis and Haemostasis 01/2004; 90(6):1046-53. · 5.76 Impact Factor
  • Thrombosis and Haemostasis 01/2003; · 5.76 Impact Factor
  • Marie-Gabrielle Pernollet, Jaroslav Kunes, Josef Zicha, Marie-Aude Devynck
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    ABSTRACT: Prague hereditary hypertriglyceridemic (HTG) rats constitute a genetic model of hypertension associated with hyperlipidemia and insulin resistance. Various cell alterations, including changes in membrane dynamics, ion transport, and decreased platelet responses to thrombin have been observed in this strain. As hypertriglyceridemia appears to be associated with reduced endothelium-dependent vasodilation and platelet aggregation, we examined whether triglycerides could modulate cell responsiveness through changes in cyclic nucleotides in platelets of HTG rats. From the age of 6 weeks, these hypertensive animals were subjected for 10 weeks to interventions that modified circulating triglycerides levels (2.17±0.09 mmol/l), leading to their reduction (gemfibrozil treatment, 0.87±0.05 mmol/l) or elevation (high fructose intake, 3.23±0.07 mmol/l). Basal cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) contents were 15% and 48% lower in isolated platelets of HTG rats than in those of Lewis controls. cAMP level was further reduced in HTG rats subjected to high fructose intake. Irrespective of their plasma triglyceride levels, the thrombin-induced increase in platelet cGMP levels present in Lewis rats was absent in platelets of HTG rats. In contrast, no strain- or treatment-related differences were observed in the magnitude or kinetics of cGMP response to exogenous nitric oxide (NO). NO-induced cGMP and cAMP changes were associated in an opposite manner with trimethylamino-diphenylhexatriene (TMA-DPH) anisotropy, a biophysical parameter that reflects the microviscosity of the outer part of the cell membrane. Our results indicate that the attenuation of platelet responsiveness to thrombin in HTG rats represents a strain difference that cannot merely be due to a difference in plasma triglyceride levels. Platelet hyporesponsiveness to agonists such as thrombin in HTG rats cannot be explained by a change in levels of inhibitory cyclic nucleotides, since they were actually found to be low and not high.
    Thrombosis Research 10/2001; 104(1):29-37. · 2.43 Impact Factor
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    ABSTRACT: Objective: To search for alterations of cytosolic pH and cell calcium handling in platelets and erythrocytes of Dahl rats susceptible and resistant to salt-induced hypertension. Design and methods: Blood pressure, plasma lipids, platelet cytosolic calcium concentration ([Ca2+]i) and pH (pHi) together with thrombin-induced changes in these parameters as well as erythrocyte [Ca2+]iand45Ca influx were determined in Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats aged 9, 15 and 24 weeks, which were fed a low-salt diet (0.3% NaCl), and in animals fed high-salt diet (4% NaCl) for 5-10 weeks since weaning. Results: With a low salt intake platelet pHiwas lower in SS/Jr than it was in SR/Jr rats, whereas basal platelet [Ca2+]iwas similar in rats of both strains. The difference in basal pHibetween SS/Jr and SR/Jr rats increased progressively with age of animals. A high salt intake from youth did not influence platelet [Ca2+]iin rats of either strain but it caused an earlier decrease in pHiin SR/Jr than it did in SS/Jr rats. Thrombin stimulation induced similar elevations of pHiand [Ca2+]iin rats of both strains, irrespective of age, salt intake and response of blood pressure to salt intake. Erythrocyte45Ca influx and [Ca2+]iwere greater for SS/Jr rats but only the latter parameter was correlated positively to blood pressure. Both regulation of platelet pHiand erythrocyte Ca2+ handling were significantly related to plasma lipid levels. Conclusions: Platelets of SS/Jr rats fed a low-salt diet were characterized by a lower basal cytosolic pHibut unchanged [Ca2+]irelative to those of SR/Jr rats. Hypertension induced by high salt intake was associated with increased erythrocyte [Ca2+]ibut not with elevation of platelet [Ca2+]ior alteration of response to stimulation with thrombin.
    Journal of Hypertension 11/1997; 15(12):1715-1721. · 4.22 Impact Factor