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

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

Author Fernandes Bertocchi, Ana Paula Autor UNIFESP Google Scholar
Campanhole, Gabriela Autor UNIFESP Google Scholar
Mei Wang, Pamella Huey Autor UNIFESP Google Scholar
Goncalves, Giselle Martins Autor UNIFESP Google Scholar
Damiao, Marcio Jose Autor UNIFESP Google Scholar
Cenedeze, Marcos Antonio Autor UNIFESP Google Scholar
Beraldo, Felipe Caetano Google Scholar
Antunes Teixeira, Vicente de Paula Google Scholar
Reis, Marlene Antonia dos Google Scholar
Mazzali, Marilda Google Scholar
Pacheco-Silva, Alvaro Autor UNIFESP Google Scholar
Saraiva Camara, Niels Olsen Autor UNIFESP Google Scholar
Institution Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Universidade Estadual de Campinas (UNICAMP)
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.
Keywords galectin-3
IL-1 beta
ischemia and reperfusion injury
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Grant number FAPESP: 04/08311-6
FAPESP: 04/13826-5
Date 2008-10-01
Published in Transplant International. Malden: Wiley-Blackwell, v. 21, n. 10, p. 999-1007, 2008.
ISSN 0934-0874 (Sherpa/Romeo, impact factor)
Publisher Wiley-Blackwell
Extent 999-1007
Origin http://dx.doi.org/10.1111/j.1432-2277.2008.00705.x
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000259087800012
URI http://repositorio.unifesp.br/handle/11600/30919

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