Mechanisms underlying the inhibitory effects of lipopolysaccharide on human platelet adhesion

dc.creatorMorganti, RP
dc.creatorCardoso, MHM
dc.creatorPereira, FG
dc.creatorLorand-Metze, I
dc.creatorDe Nucci, G
dc.creatorMarcondes, S
dc.creatorAntunes, E
dc.date2010
dc.date2014-11-20T01:24:07Z
dc.date2015-11-26T17:11:17Z
dc.date2014-11-20T01:24:07Z
dc.date2015-11-26T17:11:17Z
dc.date.accessioned2018-03-28T23:59:48Z
dc.date.available2018-03-28T23:59:48Z
dc.identifierPlatelets. Taylor & Francis Ltd, v. 21, n. 4, n. 260, n. 269, 2010.
dc.identifier0953-7104
dc.identifierWOS:000279900800004
dc.identifier10.3109/09537101003637240
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53534
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/53534
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53534
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281064
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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 mu g/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 mu g/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.description4
dc.description260
dc.description269
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherTaylor & Francis Ltd
dc.publisherAbingdon
dc.publisherInglaterra
dc.relationPlatelets
dc.relationPlatelets
dc.rightsfechado
dc.rightshttp://journalauthors.tandf.co.uk/permissions/reusingOwnWork.asp
dc.sourceWeb of Science
dc.subjectPlatelet adhesion
dc.subjectfibrinogen
dc.subjectcalcium mobilization
dc.subjectreactive-oxygen species
dc.subjectProteus-mirabilis Lipopolysaccharide
dc.subjectEscherichia-coli Lipopolysaccharide
dc.subjectNitric-oxide Synthase
dc.subjectToll-like Receptor-4
dc.subjectAntiplatelet Activity
dc.subjectSignal-transduction
dc.subjectBlood-platelets
dc.subjectExpression
dc.subjectEndotoxin
dc.subjectAggregation
dc.titleMechanisms underlying the inhibitory effects of lipopolysaccharide on human platelet adhesion
dc.typeArtículos de revistas


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