Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/55165
Type: Artigo de periódico
Title: Attenuation of glycerol-induced acute kidney injury by previous partial hepatectomy: Role of hepatocyte growth factor/c-met axis in tubular protection
Author: Homsi, E
Janino, P
Biswas, SK
Mizuno, S
Nakamura, T
de Faria, JBL
Abstract: Background/Aims: Previous partial hepatectomy (HPTX) can attenuate glycerol-induced acute kidney injury (GlyAKI). The aim of this study was to explore the pathophysiological mechanisms and the role of hepatocyte growth factor (HGF) in kidney protection. Methods: Rats were subjected to HPTX 24 h before glycerol administration. Renal function, acute tubular necrosis, apoptosis, leukocyte infiltration, and the expression of HGF, c-met, monocyte chemoattractant protein-1, interleukin-1 beta, and heme oxygenase-1 were evaluated 24 h after glycerol injection. The regenerative response was analyzed from 6 to 72 h after glycerol injection (BrdU incorporation). In a separate series of experiments, Gly-AKI+HPTX rats were treated with antiHGF antibody. Results: Gly-AKI+ HPTX rats showed an increased expression of renal HGF and c-met as well as an improved creatinine clearance and reduced acute tubular necrosis and apoptosis, cytokine expression, and leukocyte infiltration. The regenerative response was less intense 24 and 72 h after glycerol administration in this group. The anti-HGF treatment disclosed an important role of HGF in the reduction of tubular injury, particularly apoptosis. Overexpression of heme oxygenase-1 was observed in Gly-AKI+ HPTX rats, but was not associated with HPTX-induced renal protection. Conclusion: We conclude that Gly-AKI+ HPTX rats have a reduced susceptibility to renal injury instead of an increased regenerative response and that endogenous HGF overexpression is responsible for suppression of tubular apoptosis. Copyright (C) 2007 S. Karger AG, Basel.
Subject: acute kidney injury
acute renal failure
hepatocyte growth factor
hepatocyte growth factor receptor c-met
apoptosis
inflammation
heme oxygenase
Country: Suíça
Editor: Karger
Rights: fechado
Identifier DOI: 10.1159/000109828
Date Issue: 2007
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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