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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampDe Nucci, Gilbertopt_BR
dc.contributor.authorunicampMarcondes, Sisipt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.typeArtigopt_BR
dc.titleThe role of superoxide anion in the inhibitory effect of SIN-1 in thrombin-activated human platelet adhesionpt_BR
dc.contributor.authorMurad, F.pt_BR
dc.contributor.authorLilla, S.pt_BR
dc.contributor.authorDe Nucci, G.pt_BR
dc.contributor.authorMarcondes, S.pt_BR
dc.contributor.authorCardoso, M.H.M.pt_BR
dc.contributor.authorAntunes, E.pt_BR
dc.contributor.authorMorganti, R.P.pt_BR
dc.subjectNitraçãopt_BR
dc.subjectPlaquetas (Sangue)pt_BR
dc.subjectÁcido peroxinitrosopt_BR
dc.subject.otherlanguageNitrationpt_BR
dc.subject.otherlanguagePeroxynitrous acidpt_BR
dc.subject.otherlanguageBlood plateletspt_BR
dc.description.abstractReactive oxygen species have an important role in the control of platelet activity. Superoxide anion (O(2)(-)) is a free radical that can be converted into other reactive oxygen species such as peroxynitrite (ONOO(-)) that is formed from the reaction between O(2)(-) and nitric oxide (NO). There are conflicting data on ONOO(-) effects in platelets because it presents pro- or anti-aggregatory actions. 3-morpholinosydnonimine (SIN-1) co-generates NO and O(2)(-), yielding ONOO(-). Therefore, the present study aimed to investigate the mechanisms involved in the inhibition of human platelet adhesion by SIN-1. Microtiter plates were coated with human fibrinogen, after which washed platelets (6 x 10(8) platelets/ml) were added to adhere. Exposure of non-activated and thrombin-activated platelets to SIN-1 (0.001-100 mu M) concentration-dependently inhibited adhesion, which was accompanied by marked increases in the cyclic GMP levels. In non-activated platelets, the soluble guanylate cyclase inhibitor ODQ prevented the SIN-1 -induced cGMP elevations and adhesion inhibition. In thrombin-activated platelets, ODQ fully prevented the SIN-1-induced cGMP elevations, but only partly prevented the adhesion inhibition. The O(2)(-) and ONOO(-) scavengers superoxide dismutase (SOD) and -(-)epigallocatechin gallate, respectively, had minimal effects in non-activated platelets. The inhibition of activated platelets by SIN-1 1 was reversed by SOD and partly reduced by ECG. Western blot analysis of SIN-1-treated platelets showed a single 105 kDa-nitrated band. Nanospray LC-MS-MS identified the protein containing 3-nitrotyrosine residues as human alpha-actinin-1-cytoskeletal isoform. Our data show that platelet adhesion inhibition by SIN-1 in activated platelets involves cGMP-independent mechanism through O(2)(-) generation. Superoxide anion signaling pathway includes ONOO(-) formation and alpha-actinin nitrationpt
dc.relation.ispartofEuropean journal of pharmacologypt_BR
dc.relation.ispartofabbreviationEur. j. pharmacol.pt_BR
dc.publisher.cityAmsterdam pt_BR
dc.publisher.countryPaíses Baixospt_BR
dc.publisherElsevierpt_BR
dc.date.issued2010pt_BR
dc.date.monthofcirculationFeb.pt_BR
dc.identifier.citationEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 627, n. 41699, n. 229, n. 234, 2010.pt_BR
dc.language.isoengpt_BR
dc.description.volume627pt_BR
dc.description.issuenumber1-3pt_BR
dc.description.firstpage229pt_BR
dc.description.lastpage234pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0014-2999pt_BR
dc.identifier.eissn1879-0712pt_BR
dc.identifier.doi10.1016/j.ejphar.2009.10.060pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S001429990900973Xpt_BR
dc.description.sponsorshipCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESpt_BR
dc.description.sponsorship1CAPES – COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2014-11-16T06:49:50Z
dc.date.available2015-11-26T16:20:46Z-
dc.date.accessioned2014-11-16T06:49:50Z
dc.date.accessioned2015-11-26T16:20:46Z-
dc.description.provenanceMade available in DSpace on 2014-11-16T06:49:50Z (GMT). No. of bitstreams: 1 WOS000274093800034.pdf: 538632 bytes, checksum: 27d2a8f0e78bfd6709003352609d5388 (MD5) Previous issue date: 2010 Bitstreams deleted on 2020-05-18T20:40:51Z: WOS000274093800034.pdf,. Added 1 bitstream(s) on 2020-05-19T14:30:34Z : No. of bitstreams: 2 000274093800034.pdf: 612933 bytes, checksum: ab0db6b1f48d185dc8a27a3cff319f0e (MD5) WOS000274093800034.pdf.txt: 36894 bytes, checksum: 07a45ce8610adf504f5da46197078c19 (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T16:20:46Z (GMT). No. of bitstreams: 2 WOS000274093800034.pdf: 538632 bytes, checksum: 27d2a8f0e78bfd6709003352609d5388 (MD5) WOS000274093800034.pdf.txt: 36894 bytes, checksum: 07a45ce8610adf504f5da46197078c19 (MD5) Previous issue date: 2010en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/72404pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/72404
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/72404-
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000274093800034-
dc.creator.orcid0000-0002-4346-7941pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.type.formArtigo originalpt_BR
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