Cytoplasmic free calcium mobilization in platelets, expression of P-selectin, phosphatidylserine, and microparticle formation, measured by whole blood flow cytometry, in hypertensive patients. Effect of doxazosin GITS

Labiós, Manuel; Martı́nez, Marcial; Gabriel, Franck; Guiral, Victoria; Ruiz-Aja, S; Aznar, Justo

doi:10.1016/j.thromres.2005.03.012

Cited by 20 publications

(12 citation statements)

References 32 publications

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“…Labiós et al demonstrated that treatment of hypertensive patients with doxazosin leads to normalization of the kinetics of cytoplasmic cytoplasmic-free calcium, leading to a reduced release of MPs. 70 Further study is needed to confirm whether the pharmacological modulation of procoagulant MP release may improve the clinical outcomes of patients with atherothrombotic disorders.…”

Section: Calcium Channels Ions and Microparticle Formationmentioning

confidence: 99%

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Morel

Jesel

Freyssinet

et al. 2011

ATVB

467

405

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Abstract-Microparticles (MPs) derived from platelets, monocytes, endothelial cells, red blood cells, and granulocytes may be detected in low concentrations in normal plasma and at increased levels in atherothrombotic cardiovascular diseases. The elucidation of the cellular mechanisms underlying the generation of circulating MPs is crucial for improving our understanding of their pathophysiological role in health and disease. The flopping of phosphatidylserine (PS) to the outer leaflet of the plasma membrane is the key event that will ultimately lead to the shedding of procoagulant MPs from activated or apoptotic cells. Research over the last few years has revealed important roles for calcium-, mitochondrial-, and caspase-dependent mechanisms leading to PS exposure. The study of Scott cells has unraveled different molecular mechanisms that may contribute to fine-tuning of PS exposure and MP release in response to a variety of specific stimuli. The pharmacological modulation of MP release may have a substantial therapeutic impact in the management of atherothrombotic vascular disorders. Because PS exposure is a key feature in pathological processes different from hemostasis and thrombosis, the most important obstacle in the field of MP-modulating drugs seems to be carefully targeting MP release to relevant cell types at an optimal level, so as to achieve a beneficial action and limit possible adverse effects. (Arterioscler Thromb Vasc Biol. 2011;31:15-26.)

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Section: Calcium Channels Ions and Microparticle Formationmentioning

confidence: 99%

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Morel

Jesel

Freyssinet

et al. 2011

ATVB

467

405

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“…Cytoplasmic free calcium mobilization was evaluated according to Labiós et al 29 Briefly, CD61PE (specific monoclonal antibody to platelet GPIIIa, Pharmingen) and 250 AM fluo-3-acetoxymethyl ester (FLUO 3-AM, calcium probe, Molecular Probes, Leiden, the Netherlands) were added to the sample. The basal fluorescence intensity corresponding to FLUO 3-AM (FL1 log) was measured for 15 seconds in the platelet population identified in the gate forward scat log/side scat log as CD61-positive events.…”

Section: Cytoplasmic Free Calcium Mobilizationmentioning

confidence: 99%

Inherited Human gp91 ^phox Deficiency Is Associated With Impaired Isoprostane Formation and Platelet Dysfunction

Pignatelli

Carnevale

Santo

et al. 2011

ATVB

128

185

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Object-Platelet isoprostane 8-ISO-prostaglandin F2␣ (8-iso-PGF2␣), a proaggregating molecule, is believed to derive from nonenzymatic oxidation of arachidonic acid. We hypothesized that NADPH is implicated in isoprostane formation and platelet activation. Methods and Results-We studied 8-iso-PGF2␣ in platelets from 8 male patients with hereditary deficiency of gp91 phox , the catalytic subunit of NADPH oxidase, and 8 male controls. On stimulation, platelets from controls produced 8-iso-PGF2␣, which was inhibited Ϫ8% by aspirin and Ϫ58% by a specific inhibitor of gp91 phox . Platelets from patients with gp91phox hereditary deficiency had normal thromboxane A 2 formation but marked 8-iso-PGF2␣ reduction compared with controls. In normal platelets incubated with a gp91 phox inhibitor or with SQ29548, a thromboxane A 2 /isoprostane receptor inhibitor, platelet recruitment, an in vitro model of thrombus growth, was reduced by 44% and 64%, respectively; a lower effect (Ϫ17%) was seen with aspirin. Moreover, thrombus formation under shear stress (blood perfusion at the wall shear rate of 1500 s Ϫ1 ) was reduced in samples in which isoprostane formation was inhibited by NADPH oxidase inhibitors. In gp91 phox -deficient patients, agonist-induced platelet aggregation was within the normal range, whereas platelet recruitment was reduced compared with controls. Incubation of platelets from gp91 phox -deficient patients with 8-iso-PGF2␣ dose-dependently (1 to 100 pmol/L) increased platelet recruitment by mobilizing platelet Ca 2ϩ and activating gpIIb/IIIa; a further increase in platelet recruitment was detected by platelet coincubation with L-NAME, an inhibitor of NO synthase. Conclusion-This

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“…Cytoplasmic free calcium mobilization was evaluated according to Labiós et al 16 Briefly, CD61PE (specific monoclonal antibody to platelet glycoprotein IIIa; Pharmingen, San Diego, CA) and 250 AM fluo-3-acetoxymethyl ester (FLUO 3-AM; calcium probe; Molecular Probes, Leiden, the Netherlands) were added to the sample. The basal fluorescence intensity corresponding to FLUO 3-AM (FL1 log; FLUO 3-AM-FITC) was measured for 15 seconds in the platelet population identified in the gate FS log/SS log as CD61-positive events.…”

Section: Cytoplasmic Free Calcium Mobilizationmentioning

confidence: 99%

Immediate Antioxidant and Antiplatelet Effect of Atorvastatin via Inhibition of Nox2

et al. 2012

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Background-Statins exert an antithrombotic effect in patients at risk of or with acute thrombosis, but no study has investigated whether this effect is immediate and whether there is an underline mechanism. Methods and Results-Patients with hypercholesterolemia were randomly allocated to a Mediterranean diet with low cholesterol intake (Ͻ300 mg/d; nϭ15) or atorvastatin (40 mg/d; nϭ15). Oxidative stress, as assessed by serum Nox2 and urinary isoprostanes, and platelet activation, as assessed by platelet recruitment, platelet isoprostanes, and thromboxane A 2 , platelet Nox2, Rac1, p47

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Cytoplasmic free calcium mobilization in platelets, expression of P-selectin, phosphatidylserine, and microparticle formation, measured by whole blood flow cytometry, in hypertensive patients. Effect of doxazosin GITS

Cited by 20 publications

References 32 publications

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Inherited Human gp91 ^phox Deficiency Is Associated With Impaired Isoprostane Formation and Platelet Dysfunction

Immediate Antioxidant and Antiplatelet Effect of Atorvastatin via Inhibition of Nox2

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Cytoplasmic free calcium mobilization in platelets, expression of P-selectin, phosphatidylserine, and microparticle formation, measured by whole blood flow cytometry, in hypertensive patients. Effect of doxazosin GITS

Cited by 20 publications

References 32 publications

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Cellular Mechanisms Underlying the Formation of Circulating Microparticles

Inherited Human gp91 phox Deficiency Is Associated With Impaired Isoprostane Formation and Platelet Dysfunction

Immediate Antioxidant and Antiplatelet Effect of Atorvastatin via Inhibition of Nox2

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Inherited Human gp91 ^phox Deficiency Is Associated With Impaired Isoprostane Formation and Platelet Dysfunction