Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/81796
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampThomazzi, Sara Mariapt_BR
dc.contributor.authorunicampLorand-Metze, Irenept_BR
dc.contributor.authorunicampDe Nucci, Gilbertopt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.typeArtigopt_BR
dc.titleNitric oxide regulates human eosinophil adhesion mechanisms in vitro by changing integrin expression and activity on the eosinophil cell surfacept_BR
dc.title.alternativeen
dc.contributor.authorConran, N.pt_BR
dc.contributor.authorThomazzi, S.M.pt_BR
dc.contributor.authorFerreira, H.H.A.pt_BR
dc.contributor.authorLorand-Metze, I.pt_BR
dc.contributor.authorDe Nucci, G.pt_BR
dc.contributor.authorAntunes, E.pt_BR
dc.subjectEosinófilospt_BR
dc.subjectÓxido nítricopt_BR
dc.subjectGMP cíclicopt_BR
dc.subject.otherlanguageEosinophilspt_BR
dc.subject.otherlanguageNitric oxidept_BR
dc.subject.otherlanguageCyclic GMPpt_BR
dc.description.abstractThe nitric oxide synthase (NOS) inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), inhibits both rat and human eosinophil chemotaxis in vitro. Here, the role of nitric oxide (NO) in human eosinophil cell surface integrin expression and function was investigated. 2 Human peripheral blood eosinophils were treated With L-NAME (0.01 - 1.0 mM) and their adhesion to human fibronectin and serum observed. Adhesion of cells to fibronectin and serum increased by 24.0 +/-4.6 and 43.8 +/-4.7%, respectively, when eosinophils were treated with 1.0 mM L-NAME. Increased adhesion by L-NAME could be abolished when cells were co-incubated with VLA-4- and Mac-1-specific monoclonal antibodies (mAbs). 3 The NO donor, sodium nitroprusside (2.5 mM), significantly inhibited eosinophil adhesion to fibronectin and serum by 34.3 +/-4.5 and 45.2 +/-5.6%, respectively. This inhibition was accompanied by a 4 fold increase in the levels of intracellular cyclic GMP. 4 Flow cytometrical analysis demonstrated that L-NAME induced an increased expression of CD11b (Mac-1) on the eosinophil cell surface of 36.3 +/-7.4%, L-NAME had no effect upon CD49d (VLA-4) expression. 5 Treatment of human eosinophils, in vitro, with H-[1,2,4] oxadiazolo quinoxatin-1-one (ODQ) (0.1 mM), an inhibitor of soluble guanylate cyclase, also significantly increased eosinophil adhesion to fibronectin and serum by 73.5 +/- 17.9 and 91.7 +/- 12.9%, respectively. This increase in adhesion could also be inhibited by co-incubation with the Mac-1 and VLA-4-specific mAbs. 6 In conclusion, results indicate that NO, via a cyclic GMP-dependent mechanism, inhibits the adhesion of human eosinophils to the extracellular matrix (ECM). This inhibition is accompanied by a decrease in the expression and function of the eosinophil's adhesion molecules, in particular, the expression of the Mac-1 integrin and the function of the VLA-4 integrinpt
dc.relation.ispartofBritish journal of pharmacologypt_BR
dc.relation.ispartofabbreviationBr j pharmacolpt_BR
dc.publisher.cityOxfordpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherJohn Wiley & Sonspt_BR
dc.date.issued2001pt_BR
dc.date.monthofcirculationOct.pt_BR
dc.identifier.citationBritish Journal Of Pharmacology. Nature Publishing Group, v. 134, n. 3, n. 632, n. 638, 2001.pt_BR
dc.language.isoengpt_BR
dc.description.volume134pt_BR
dc.description.issuenumber3pt_BR
dc.description.firstpage632pt_BR
dc.description.lastpage638pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0007-1188pt_BR
dc.identifier.eissn1476-5381pt_BR
dc.identifier.doi10.1038/sj.bjp.0704295pt_BR
dc.identifier.urlhttps://bpspubs.onlinelibrary.wiley.com/doi/full/10.1038/sj.bjp.0704295pt_BR
dc.description.sponsorshipFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2014-11-13T17:31:02Z
dc.date.available2015-11-26T17:10:46Z-
dc.date.accessioned2014-11-13T17:31:02Z
dc.date.accessioned2015-11-26T17:10:46Z-
dc.description.provenanceMade available in DSpace on 2014-11-13T17:31:02Z (GMT). No. of bitstreams: 1 WOS000171395000020.pdf: 172448 bytes, checksum: 456288d99487aeca261590391fbbc778 (MD5) Previous issue date: 2001 Bitstreams deleted on 2020-05-18T20:41:10Z: WOS000171395000020.pdf,. Added 1 bitstream(s) on 2020-05-19T14:31:00Z : No. of bitstreams: 2 000171395000020.pdf: 256465 bytes, checksum: e954cb1570f37d7245d34e2a8ae7eb24 (MD5) WOS000171395000020.pdf.txt: 37484 bytes, checksum: db6c6a1fec40df54186b96326b65e872 (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T17:10:46Z (GMT). No. of bitstreams: 2 WOS000171395000020.pdf: 172448 bytes, checksum: 456288d99487aeca261590391fbbc778 (MD5) WOS000171395000020.pdf.txt: 37484 bytes, checksum: db6c6a1fec40df54186b96326b65e872 (MD5) Previous issue date: 2001en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81796pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/81796
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81796-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.description.abstractalternative-
dc.identifier.source000171395000020-
dc.creator.orcid0000-0003-0348-0401pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-4346-7941pt_BR
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.type.formArtigo de pesquisapt_BR
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