Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/327315
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authoremailantunes@fcm.unicamp.brpt_BR
dc.contributor.authorunicampBarbosa, Ana Paula de Limapt_BR
dc.contributor.authorunicampAnhê, Gabriel Foratopt_BR
dc.contributor.authorunicampDe Nucci, Gilbertopt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.typeArtigopt_BR
dc.titleThe Soluble Guanylyl Cyclase Activator Bay 60-2770 Inhibits Murine Allergic Airways Inflammation And Human Eosinophil Chemotaxisen
dc.titleThe soluble guanylyl cyclase activator bay 60-2770 inhibits murine allergic airways inflammation and human eosinophil chemotaxispt_BR
dc.contributor.authorBaldissera Junior, Lineupt_BR
dc.contributor.authorSquebola-Cola, Dalize M.pt_BR
dc.contributor.authorCalixto, Marina C.pt_BR
dc.contributor.authorLima-Barbosa, Ana P.pt_BR
dc.contributor.authorRenno, Andre L.pt_BR
dc.contributor.authorAnhe, Gabriel F.pt_BR
dc.contributor.authorCondino-Neto, Antoniopt_BR
dc.contributor.authorDe Nucci, Gilbertopt_BR
dc.contributor.authorAntunes, Edsonpt_BR
unicamp.authorAntunes, Edson] Univ Estadual Campinas, UNICAMP, Fac Med Sci, Dept Pharmacol, BR-13084971 Campinas, SP, Brazilpt_BR
unicamp.author.external[Baldissera, Lineu, Jr.pt_BR
unicamp.author.externalSquebola-Cola, Dalize M.pt_BR
unicamp.author.externalCalixto, Marina C.pt_BR
unicamp.author.externalLima-Barbosa, Ana P.pt_BR
unicamp.author.externalRenno, Andre L.pt_BR
unicamp.author.externalAnhe, Gabriel F.pt_BR
unicamp.author.externalCondino-Neto, Antoniopt_BR
unicamp.author.externalDe Nucci, Gilbertopt_BR
dc.subjectTh2 Cytokinesen
dc.subjectBone Marrowen
dc.subjectEotaxinen
dc.subjectCyclic Gmpen
dc.subjectInducible Nitric Oxide Synthaseen
dc.subjectMedula ósseapt_BR
dc.subjectGMP cíclicopt_BR
dc.subject.otherlanguageBone marrowpt_BR
dc.subject.otherlanguageCyclic GMPpt_BR
dc.description.abstractActivators of soluble guanylyl cyclase (sGC) act preferentially in conditions of enzyme oxidation or haem group removal. This study was designed to investigate the effects of the sGC activator BAY 60-2770 in murine airways inflammation and human eosinophil chemotaxis. Methods: C57BI/6 mice treated or not with BAY 60-2770 (1 mg/kg/day, 14 days) were intranasally challenged with ovalbumin (OVA). At 48 h, bronchoalveolar lavage fluid (BALF) was performed, and circulating blood, bone marrow and lungs were obtained. Human eosinophils purified from peripheral blood were used to evaluate the cell chemotaxis. Results: OVA-challenge promoted marked increases in eosinophil number in BAL, lung tissue, circulating blood and bone marrow, all of which were significantly reduced by BAY 60-2770. The IL-4 and IL-5 levels in BALF were significantly reduced by BAY 60-2770. Increased protein expression of iNOS, along with decreases of expression of sGC (alpha 1 and beta 1 subunits) and cGMP levels were detected in lung tissue of OVA-challenged mice. BAY 60-2770 fully restored to baseline the iNOS and sGC subunit expressions, and cGMP levels. In human isolated eosinophils, BAY 60-2770 (1-5 mu M) had no effects on the cGMP levels and eotaxin-induced chemotaxis; however, prior incubation with ODQ (10 mu M) markedly elevated the BAY 60-2770-induced cyclic GMP production, further inhibiting the eosinophil chemotaxis. Conclusions: BAY 60-2770 reduces airway eosinophilic inflammation and rescue the sGC levels. In human eosinophils under oxidized conditions, BAY 60-2770 elevates the cGMP levels causing cell chemotaxis inhibition. BAY 60-2770 may reveal a novel therapeutic target for asthma treatment. (C) 2016 Elsevier Ltd. All rights reserved.en
dc.description.abstractActivators of soluble guanylyl cyclase (sGC) act preferentially in conditions of enzyme oxidation or haem group removal. This study was designed to investigate the effects of the sGC activator BAY 60-2770 in murine airways inflammation and human eosinophil chemotaxis. Methods: C57BI/6 mice treated or not with BAY 60-2770 (1 mg/kg/day, 14 days) were intranasally challenged with ovalbumin (OVA). At 48 h, bronchoalveolar lavage fluid (BALF) was performed, and circulating blood, bone marrow and lungs were obtained. Human eosinophils purified from peripheral blood were used to evaluate the cell chemotaxis. Results: OVA-challenge promoted marked increases in eosinophil number in BAL, lung tissue, circulating blood and bone marrow, all of which were significantly reduced by BAY 60-2770. The IL-4 and IL-5 levels in BALF were significantly reduced by BAY 60-2770. Increased protein expression of iNOS, along with decreases of expression of sGC (alpha 1 and beta 1 subunits) and cGMP levels were detected in lung tissue of OVA-challenged mice. BAY 60-2770 fully restored to baseline the iNOS and sGC subunit expressions, and cGMP levels. In human isolated eosinophils, BAY 60-2770 (1-5 mu M) had no effects on the cGMP levels and eotaxin-induced chemotaxis; however, prior incubation with ODQ (10 mu M) markedly elevated the BAY 60-2770-induced cyclic GMP production, further inhibiting the eosinophil chemotaxis. Conclusions: BAY 60-2770 reduces airway eosinophilic inflammation and rescue the sGC levels. In human eosinophils under oxidized conditions, BAY 60-2770 elevates the cGMP levels causing cell chemotaxis inhibition. BAY 60-2770 may reveal a novel therapeutic target for asthma treatmentpt
dc.relation.ispartofPulmonary pharmacology & therapeuticspt_BR
dc.relation.ispartofabbreviationPulm pharmacol therpt_BR
dc.publisher.cityLondonpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherElsevierpt_BR
dc.date.issued2016pt_BR
dc.date.monthofcirculationDec.pt_BR
dc.identifier.citationPulmonary Pharmacology & Therapeutics. Academic Press Ltd- Elsevier Science Ltd, v. 41, p. 86 - 95, 2016.pt_BR
dc.language.isoengpt_BR
dc.description.volume41pt_BR
dc.description.issuenumberpt_BR
dc.description.firstpage86pt_BR
dc.description.lastpage95pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.sourceWOSpt_br
dc.identifier.issn1094-5539pt_BR
dc.identifier.eissn1522-9629pt_BR
dc.identifier.wosidWOS:000390515100010pt_BR
dc.identifier.doi10.1016/j.pupt.2016.11.001pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S1094553916301456pt_BR
dc.description.sponsorshipFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorshipCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1CNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2017-11-13T13:15:16Z-
dc.date.accessioned2017-11-13T13:15:16Z-
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dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/327315-
dc.contributor.departmentDepartamento de Ciênciaspt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeColégio Técnico de Campinaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000390515100010-
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0003-1543-4154pt_BR
dc.creator.orcid0000-0002-4346-7941pt_BR
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.type.formArtigo original-
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