A Role for galectin-3 in renal tissue damage triggered by ischemia and reperfusion injury

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dc.contributor.author Fernandes Bertocchi, Ana Paula [UNIFESP]
dc.contributor.author Campanhole, Gabriela [UNIFESP]
dc.contributor.author Mei Wang, Pamella Huey [UNIFESP]
dc.contributor.author Goncalves, Giselle Martins [UNIFESP]
dc.contributor.author Damiao, Marcio Jose [UNIFESP]
dc.contributor.author Cenedeze, Marcos Antonio [UNIFESP]
dc.contributor.author Beraldo, Felipe Caetano
dc.contributor.author Antunes Teixeira, Vicente de Paula
dc.contributor.author Reis, Marlene Antonia dos
dc.contributor.author Mazzali, Marilda
dc.contributor.author Pacheco-Silva, Alvaro [UNIFESP]
dc.contributor.author Saraiva Camara, Niels Olsen [UNIFESP]
dc.date.accessioned 2016-01-24T13:51:42Z
dc.date.available 2016-01-24T13:51:42Z
dc.date.issued 2008-10-01
dc.identifier http://dx.doi.org/10.1111/j.1432-2277.2008.00705.x
dc.identifier.citation Transplant International. Malden: Wiley-Blackwell, v. 21, n. 10, p. 999-1007, 2008.
dc.identifier.issn 0934-0874
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/30919
dc.description.abstract Ischemic-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.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 999-1007
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof Transplant International
dc.rights Acesso aberto
dc.subject galectin-3 en
dc.subject IL-1 beta en
dc.subject IL-6 en
dc.subject ischemia and reperfusion injury en
dc.subject MCP-1 en
dc.title A Role for galectin-3 in renal tissue damage triggered by ischemia and reperfusion injury en
dc.type Artigo
dc.rights.license http://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Universidade Estadual de Campinas (UNICAMP)
dc.description.affiliation Univ São Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunol, BR-05508900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, São Paulo, Brazil
dc.description.affiliation Univ Estadual Campinas, Div Nephrol, Campinas, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 04/08311-6
dc.description.sponsorshipID FAPESP: 04/13826-5
dc.identifier.doi 10.1111/j.1432-2277.2008.00705.x
dc.description.source Web of Science
dc.identifier.wos WOS:000259087800012



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