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dc.contributor.authorFernandes Bertocchi, Ana Paula [UNIFESP]
dc.contributor.authorCampanhole, Gabriela [UNIFESP]
dc.contributor.authorMei Wang, Pamella Huey [UNIFESP]
dc.contributor.authorGoncalves, Giselle Martins [UNIFESP]
dc.contributor.authorDamiao, Marcio Jose [UNIFESP]
dc.contributor.authorCenedeze, Marcos Antonio [UNIFESP]
dc.contributor.authorBeraldo, Felipe Caetano
dc.contributor.authorAntunes Teixeira, Vicente de Paula
dc.contributor.authorReis, Marlene Antonia dos
dc.contributor.authorMazzali, Marilda
dc.contributor.authorPacheco-Silva, Alvaro [UNIFESP]
dc.contributor.authorSaraiva Camara, Niels Olsen [UNIFESP]
dc.identifier.citationTransplant International. Malden: Wiley-Blackwell, v. 21, n. 10, p. 999-1007, 2008.
dc.description.abstractIschemic-reperfusion injury (IRI) triggers an inflammatory response involving neutrophils/macrophages, lymphocytes and endothelial cells. Galectin-3 is a multi-functional lectin with a broad range of action such as promotion of neutrophil adhesion, induction of oxidative stress, mastocyte migration and degranulation, and production of pro-inflammatory cytokines. the aim of this study was evaluate the role of galectin-3 in the inflammation triggered by IRI. Galectin-3 knockout (KO) and wild type (wt) mice were subjected to 45 min of renal pedicle occlusion. Blood and kidney samples were collected at 6, 24, 48 and 120 h. Blood urea was analyzed enzymatically, while MCP-1, IL-6 and IL-1 beta were studied by real-time PCR. Reactive oxygen species (ROS) was investigated by flow cytometry. Morphometric analyses were performed at 6, 24, 48 and 120 h after reperfusion. Urea peaked at 24 h, being significantly lower in knockout animals (wt = 264.4 +/- 85.21 mg/dl vs. gal-3 KO = 123.74 +/- 29.64 mg/dl, P = 0.001). Galectin-3 knockout animals presented less acute tubular necrosis and a more prominent tubular regeneration when compared with controls concurrently with lower expression of MCP-1, IL-6, IL-1 beta, less macrophage infiltration and lower ROS production at early time points. Galectin-3 seems to play a role in renal IRI involving the secretion of macrophage-related chemokine, pro-inflammatory cytokines and ROS production.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.relation.ispartofTransplant International
dc.rightsAcesso aberto
dc.subjectIL-1 betaen
dc.subjectischemia and reperfusion injuryen
dc.titleA Role for galectin-3 in renal tissue damage triggered by ischemia and reperfusion injuryen
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.description.affiliationUniv São Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunol, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, São Paulo, Brazil
dc.description.affiliationUniv Estadual Campinas, Div Nephrol, Campinas, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 04/08311-6
dc.description.sponsorshipIDFAPESP: 04/13826-5
dc.description.sourceWeb of Science

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