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Inflammation-induced modulation of cellular galectin-1 and-3 expression in a model of rat peritonitis

dc.contributor.authorGil, C. D.
dc.contributor.authorCooper, D.
dc.contributor.authorRosignoli, G.
dc.contributor.authorPerretti, M.
dc.contributor.authorOliani, S. M.
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionQueen Mary Sch Med & Dent
dc.date.accessioned2014-05-20T15:21:45Z
dc.date.available2014-05-20T15:21:45Z
dc.date.issued2006-03-01
dc.description.abstractObjective and design: To investigate the effect of galectin-1 (Gal-1) and -3 (Gal-3) on leukocyte migration and analyze the expression of both galectins in inflammatory cells using a model of rat peritonitis.Material or Subjects: Sprague-Dawley rats (n = 4 per group).Treatment: Peritonitis was induced in animals through intraperitoneal injection of carrageenin (1.5 mg/kg) and rat mesenteries were analyzed at different time points (0, 4, 24 and 48h). For pharmacological treatment, rats received intravenous injection of Gal-1 or -3 (3 mu g/kg) followed by carrageenin.Methods: Western blotting and immunoelectron microscopy analysis. Statistical analysis was performed using ANOVA followed by Bonferroni test.Results: Pharmacological treatment with Gal-1, but not Gal-3, inhibited (similar to 50%) leukocyte recruitment into the peritoneal cavity at 4h time-point. In this early phase, immunogold staining of mesenteries showed a diminished Gal-3 expression in degranulated mast cells and Gal-1 in transmigrated neutrophils (similar to 20% reduction compared to intravascular cells). In the later phases (24 and 48 h), leukocyte turnover was associated with augmented Gal-1 expression in neutrophils and macrophages and Gal-3 in mast cells and macrophages.Conclusions: These results point to a balanced expression of cell-associated-Gal-1/Gal-3 and might impact on the development of new therapeutic strategies for inflammatory diseases.en
dc.description.affiliationUNESP, Dept Biol, Inst Biociencias Letras & Ciências Exatas, BR-15054000 Sao Jose do Rio Preto, SP, Brazil
dc.description.affiliationFAMERP, Fac Med, Dept Agron, BR-15090000 Sao Jose do Rio Preto, SP, Brazil
dc.description.affiliationUNIFESP, São Paulo Sch Med, Postgrad Morphol, BR-04023900 São Paulo, Brazil
dc.description.affiliationQueen Mary Sch Med & Dent, William Harvey Res Inst, London ECIM 6BQ, England
dc.description.affiliationUnespUNESP, Dept Biol, Inst Biociencias Letras & Ciências Exatas, BR-15054000 Sao Jose do Rio Preto, SP, Brazil
dc.format.extent99-107
dc.identifierhttp://dx.doi.org/10.1007/s00011-005-0059-4
dc.identifier.citationInflammation Research. Basel: Birkhauser Verlag Ag, v. 55, n. 3, p. 99-107, 2006.
dc.identifier.doi10.1007/s00011-005-0059-4
dc.identifier.issn1023-3830
dc.identifier.lattes5102737730539655
dc.identifier.urihttp://hdl.handle.net/11449/32873
dc.identifier.wosWOS:000236559700003
dc.language.isoeng
dc.publisherBirkhauser Verlag Ag
dc.relation.ispartofInflammation Research
dc.relation.ispartofjcr2.990
dc.relation.ispartofsjr1,062
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectIn vivo inflammationpt
dc.subjectmast cellpt
dc.subjectneutrophilpt
dc.subjectendothelial cellpt
dc.subjectmacrophagept
dc.titleInflammation-induced modulation of cellular galectin-1 and-3 expression in a model of rat peritonitisen
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights
dcterms.rightsHolderBirkhauser Verlag Ag
dspace.entity.typePublication
unesp.author.lattes5102737730539655
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências Letras e Ciências Exatas, São José do Rio Pretopt
unesp.departmentBiologia - IBILCEpt

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