title: Endogenous hepatocyte growth factor attenuates inflammatory response in glycerol-induced acute kidney injury.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Nephrology, Department of Medicine, School of Medical Sciences, State University of Campinas, São Paulo, Brazil. ehomsi@aclnet.com.br
authors.forename: Eduardo
authors.initials: E
authors.lastname: Homsi
authors.forename: Patricia
authors.initials: P
authors.lastname: Janino
authors.forename: Mariane
authors.initials: M
authors.lastname: Amano
authors.forename: Niels Olsen
authors.initials: NO
authors.lastname: Saraiva Camara
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D050990:GATA3 Transcription Factor / Q000235:genetics; D015870:Gene Expression / Q000502:physiology; D005990:Glycerol / Q000633:toxicity; D017228:Hepatocyte Growth Factor / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D016753:Interleukin-10 / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D007684:Kidney Tubules / Q000502:physiology; D008297:Male; D019859:Proto-Oncogene Proteins c-met / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D020825:T-Box Domain Proteins / Q000235:genetics; D018417:Th1 Cells / Q000473:pathology; D018418:Th2 Cells / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D000098815:T-bet Transcription Factor
chemical_list: D000906:Antibodies; D050990:GATA3 Transcription Factor; D053583:Interleukin-1beta; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D017228:Hepatocyte Growth Factor; D019859:Proto-Oncogene Proteins c-met; D005990:Glycerol