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Am J Nephrol. 2009;29(4):283-91. doi: 10.1159/000159275. Epub 2008 Sep 29.

Endogenous hepatocyte growth factor attenuates inflammatory response in glycerol-induced acute kidney injury.

Author information

1
Division of Nephrology, Department of Medicine, School of Medical Sciences, State University of Campinas, São Paulo, Brazil. ehomsi@aclnet.com.br

Abstract

BACKGROUND:

Hepatocyte growth factor (HGF) is overexpressed after acute kidney injury (AKI). The aim of this study was to evaluate the role of endogenous HGF in the progression of the inflammatory response in glycerol-induced AKI (Gly-AKI) in rats.

METHODS:

Renal and systemic HGF expressions were evaluated during the development of Gly-AKI. Subsequently, the blockade of endogenous HGF was analyzed in rats treated with anti-HGF antibody concomitant to glycerol injection. Apoptosis, cell infiltration and chemokine and cytokine profiles were investigated.

RESULTS:

We detected an early peak of renal and plasma HGF protein expressions 3 h after glycerol injection. The pharmacological blockade of the endogenous HGF exacerbated the renal impairment, the tubular apoptosis, the renal expression of monocyte chemoattractant protein-1 and the macrophage, CD43+, CD4+ and CD8+ T lymphocytes renal infiltration. The analysis of mRNA expressions of Th1 (t-bet, TNF-alpha, IL-1beta) and Th2 (gata-3, IL-4, IL-10) cytokines showed a Th1-polarized response in Gly-AKI rats that was aggravated with the anti-HGF treatment.

CONCLUSION:

Endogenous HGF attenuates the renal inflammatory response, leukocyte infiltration and Th1 polarization after glycerol injection. The control of cellular immune response may partly explain the protective effect of endogenous HGF in the development of Gly-AKI.

PMID:
18824844
DOI:
10.1159/000159275
[Indexed for MEDLINE]

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