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

  1. Ana Paula Fernandes Bertocchi1,
  2. Gabriela Campanhole1,
  3. Pamella Huey Mei Wang1,
  4. Giselle Martins Gonçalves1,
  5. Márcio José Damião1,
  6. Marcos Antônio Cenedeze1,
  7. Felipe Caetano Beraldo2,
  8. Vicente De Paula Antunes Teixeira3,
  9. Marlene Antônia Dos Reis3,
  10. Marilda Mazzali2,
  11. Alvaro Pacheco-Silva1,
  12. Niels Olsen Saraiva Câmara1,4

Article first published online: 24 JUL 2008

DOI: 10.1111/j.1432-2277.2008.00705.x

Issue

Transplant International

Transplant International

Volume 21, Issue 10, pages 999–1007, October 2008

Additional Information

How to Cite

Fernandes Bertocchi, A. P., Campanhole, G., Wang, P. H. M., Gonçalves, G. M., Damião, M. J., Cenedeze, M. A., Beraldo, F. C., De Paula Antunes Teixeira, V., Dos Reis, M. A., Mazzali, M., Pacheco-Silva, A. and Câmara, N. O. S. (2008), A Role for galectin-3 in renal tissue damage triggered by ischemia and reperfusion injury. Transplant International, 21: 999–1007. doi: 10.1111/j.1432-2277.2008.00705.x

Author Information

  1. 1

     Laboratory of Clinical and Experimental Immunology, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil

  2. 2

     Division of Nephrology, Universidade Estudal de Campinas, Campinas, Brazil

  3. 3

     Department of Pathology, Universidade Federal de Uberaba, Minas Gerais, Brazil

  4. 4

     Laboratory for Transplantation Immunology, Department of Immunology, Universidade de São Paulo, São Paulo, Brazil

*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

Publication History

  1. Issue published online: 9 SEP 2008
  2. Article first published online: 24 JUL 2008
  3. Received: 10 December 2007 Revision requested: 8 January 2008 Accepted: 9 May 2008

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Keywords:

  • galectin-3;
  • IL-1β;
  • IL-6;
  • ischemia and reperfusion injury;
  • MCP-1

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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