Annexin 1 mimetic peptide protects against renal ischemia/reperfusion injury in rats
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Data
2011-01-01
Autores
Facio, Fernando N.
Sena, Angela A. [UNESP]
Araujo, Leandro P. [UNESP]
Mendes, Gloria E.
Castro, Isac
Luz, Marcus A. M.
Yu, Luis
Oliani, Sonia Maria [UNESP]
Burdmann, Emmanuel A.
Título da Revista
ISSN da Revista
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Editor
Springer
Resumo
Inflammation is currently recognized as a key mechanism in the pathogenesis of renal ischemia-reperfusion (I/R) injury. The importance of infiltrating neutrophil, lymphocytes, and macrophage in this kind of injury has been assessed with conflicting results. Annexin 1 is a protein with potent neutrophil anti-migratory activity. In order to evaluate the effects of annexin A1 on renal I/R injury, uninephrectomized rats received annexin A1 mimetic peptide Ac2-26 (100 mu g) or vehicle before 30 min of renal artery clamping and were compared to sham surgery animals. Annexin A1 mimetic peptide granted a remarkable protection against I/R injury, preventing glomerular filtration rate and urinary osmolality decreases and acute tubular necrosis development. Annexin A1 infusion aborted neutrophil extravasation and attenuated macrophage infiltration but did not prevent tissue lymphocyte traffic. I/R increased annexin A1 expression (assessed by transmission electron microscopy) in renal epithelial cells, which was attenuated by exogenous annexin A1 infusion. Additionally, annexin A1 reduced I/R injury in isolated proximal tubules suspension. Annexin A1 protein afforded striking functional and structural protection against renal I/R. These results point to an important role of annexin A1 in the epithelial cells defense against I/R injury and indicate that neutrophils are key mediators for the development of tissue injury after renal I/R. If these results were confirmed in clinical studies, annexin A1 might emerge as an important tool to protect against I/R injury in renal transplantation and in vascular surgery.
Descrição
Palavras-chave
Annexin A1, Acute kidney injury, Ischemia/reperfusion injury, Kidney, Neutrophils, Acute tubular necrosis
Como citar
Journal of Molecular Medicine-jmm. New York: Springer, v. 89, n. 1, p. 51-63, 2011.