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Attenuation of glycerol-induced acute kidney injury by previous partial hepatectomy: role of hepatocyte growth factor/c-met axis in tubular protection.

AbstractBACKGROUND/AIMS:
Previous partial hepatectomy (HPTX) can attenuate glycerol-induced acute kidney injury (Gly-AKI). 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-1beta, 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 anti-HGF 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.
AuthorsEduardo Homsi, Patricia Janino, Subrata K Biswas, Shinya Mizuno, Toshikazu Nakamura, Jose B Lopes de Faria
JournalNephron. Experimental nephrology (Nephron Exp Nephrol) Vol. 107 Issue 3 Pg. e95-106 ( 2007) ISSN: 1660-2129 [Electronic] Switzerland
PMID17940345 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 2007 S. Karger AG, Basel.
Chemical References
  • Ccl2 protein, rat
  • Chemokine CCL2
  • Interleukin-1
  • RNA, Messenger
  • Hepatocyte Growth Factor
  • Creatinine
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat
  • Proto-Oncogene Proteins c-met
  • Glycerol
Topics
  • Animals
  • Apoptosis (drug effects)
  • Chemokine CCL2 (biosynthesis, genetics)
  • Creatinine (blood)
  • Gene Expression Regulation
  • Glycerol (toxicity)
  • Heme Oxygenase (Decyclizing) (biosynthesis, genetics)
  • Hepatectomy
  • Hepatocyte Growth Factor (biosynthesis, genetics, physiology)
  • Interleukin-1 (biosynthesis, genetics)
  • Kidney (metabolism, physiopathology)
  • Kidney Tubular Necrosis, Acute (chemically induced, metabolism, pathology, prevention & control, surgery)
  • Macrophages (pathology)
  • Proto-Oncogene Proteins c-met (biosynthesis, genetics, physiology)
  • RNA, Messenger (biosynthesis, genetics)
  • Rats
  • Rats, Wistar
  • Regeneration
  • T-Lymphocytes (pathology)

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