dc.creatorMorganti, Rafael P
dc.creatorCardoso, Marcia H M
dc.creatorPereira, Fernanda G
dc.creatorLorand-Metze, Irene
dc.creatorDe Nucci, Gilberto
dc.creatorMarcondes, Sisi
dc.creatorAntunes, Edson
dc.date2010
dc.date2015-11-27T13:17:38Z
dc.date2015-11-27T13:17:38Z
dc.date.accessioned2018-03-29T01:10:30Z
dc.date.available2018-03-29T01:10:30Z
dc.identifierPlatelets. v. 21, n. 4, p. 260-9, 2010.
dc.identifier1369-1635
dc.identifier10.3109/09537101003637240
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/20218907
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/198751
dc.identifier20218907
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1298984
dc.descriptionAlterations in platelet aggregation in septic conditions are well established. However, little is known about the effects of lipopolysaccharide (LPS) on platelet adhesion. We have therefore investigated the effects of LPS in human platelet adhesion, using an in vitro model of platelet adhesion to fibrinogen-coated wells. Microtiter plates were coated with human fibrinogen, after which washed platelets (6 x 10(8) platelets/ml) were allowed to adhere. Adherent platelets were quantified through measurement of acid phosphatase activity. Calcium mobilization in Fura2-AM-loaded platelets was monitored with a spectrofluorimeter. Platelet flow cytometry in thrombin-stimulated platelets was performed using monoclonal mouse anti-platelet GPIIb/IIIa antibody (PAC-1). Prior incubation of washed platelets with LPS (0.01-300 microg/ml) for 5 to 60 min concentration- and time-dependently inhibited non-activated platelet adhesion. In thrombin-activated (50 mU/ml) platelets, LPS inhibited the adhesion to a significantly lesser extent than non-activated platelets. Cyclohexamide, superoxide dismutase polyethylene glycol (PEG-SOD) or catalase polyethylene glycol did not affect the LPS responses. No alterations in cyclic GMP levels were seen after platelet incubation with LPS, except with the highest concentration employed (300 microg/ml) where an increase of 36% (P < 0.05) was observed. Thrombin increased by 7.5-fold the internal Ca(2+) platelet levels, an effect markedly inhibited by LPS. Thrombin induced concentration-dependent platelet GPIIb/IIIa activation, but LPS failed to affect the activation state of this membrane glycoprotein. In conclusion, LPS inhibits human platelet adhesion to fibrinogen by mechanisms involving blockade of external Ca(2+), independently of cGMP generation and activation of GPIIb/IIIa complex.
dc.description21
dc.description260-9
dc.languageeng
dc.relationPlatelets
dc.relationPlatelets
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAcid Phosphatase
dc.subjectAnimals
dc.subjectBlood Platelets
dc.subjectCalcium
dc.subjectCatalase
dc.subjectCells, Cultured
dc.subjectCyclic Gmp
dc.subjectCycloheximide
dc.subjectDual Specificity Phosphatase 2
dc.subjectFibrinogen
dc.subjectHumans
dc.subjectLipopolysaccharides
dc.subjectMice
dc.subjectPlatelet Adhesiveness
dc.subjectPlatelet Function Tests
dc.subjectPlatelet Glycoprotein Gpiib-iiia Complex
dc.subjectProtein Synthesis Inhibitors
dc.subjectReactive Oxygen Species
dc.subjectSuperoxide Dismutase
dc.titleMechanisms Underlying The Inhibitory Effects Of Lipopolysaccharide On Human Platelet Adhesion.
dc.typeArtículos de revistas


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