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

Authors

  • Ana Paula Fernandes Bertocchi,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Gabriela Campanhole,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Pamella Huey Mei Wang,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Giselle Martins Gonçalves,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Márcio José Damião,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Marcos Antônio Cenedeze,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Felipe Caetano Beraldo,

    1.  Division of Nephrology, Universidade Estudal de Campinas, Campinas, Brazil
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  • Vicente De Paula Antunes Teixeira,

    1.  Department of Pathology, Universidade Federal de Uberaba, Minas Gerais, Brazil
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  • Marlene Antônia Dos Reis,

    1.  Department of Pathology, Universidade Federal de Uberaba, Minas Gerais, Brazil
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  • Marilda Mazzali,

    1.  Division of Nephrology, Universidade Estudal de Campinas, Campinas, Brazil
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  • Alvaro Pacheco-Silva,

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
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  • Niels Olsen Saraiva Câmara

    1.  Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil
    2.  Laboratory for Transplantation Immunology, Department of Immunology, Universidade de São Paulo, São Paulo, Brazil
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Niels Olsen Saraiva Câmara, MD, PhD, Department of Immunology, Institute of Biomedical Science IV, Universidade de São Paulo, Rua Prof Lineu Prestes, 1730, 05508-900 São Paulo, SP, Brazil. Tel.: 5511 3091 7388; fax: 5511 3091 7224; e-mail: niels@icb.usp.br

Summary

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-1β 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-1β, 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.

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