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

Author(s):Show less -

Fernandes Bertocchi, Ana Paula ^[1] ; Campanhole, Gabriela ^[1] ; Mei Wang, Pamella Huey ^[1] ; Goncalves, Giselle Martins ^[1] ; Damiao, Marcio Jose ^[1] ; Cenedeze, Marcos Antonio ^[1] ; Beraldo, Felipe Caetano ^[2] ; Antunes Teixeira, Vicente de Paula ; dos Reis, Marlene Antonia ; Mazzali, Marilda ^[2] ; Pacheco-Silva, Alvaro ^[1] ; Saraiva Camara, Niels Olsen ^{[1, 3]}

Affiliation

^[1] Univ Fed Sao Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, Sao Paulo - Brazil

^[2] Univ Estadual Campinas, Div Nephrol, Campinas - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunol, BR-05508900 Sao Paulo - Brazil

• Document type: Journal article
• Source: Transplant International; v. 21, n. 10, p. 999-1007, OCT 2008.
• Web of Science Citations: 43

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. (AU)

• FAPESP's process: 04/08311-6 - Molecular, cellular and pathophysiological mechanisms on acute renal failure
• Grantee: Nestor Schor
• Support Opportunities: Research Projects - Thematic Grants