title: IF/TA-related metabolic changes--proteome analysis of rat renal allografts.
abstract: BACKGROUND
  Chronic allograft nephropathy, now more specifically termed interstitial fibrosis and tubular atrophy without evidence of any specific aetiology (IF/TA), is still an important cause of late graft loss. There is no effective therapy for IF/TA, in part due to the disease's multifactorial nature and its incompletely understood pathogenesis.
  
  
  METHODS
  We used a differential in-gel electrophoresis and mass spectrometry technique to study IF/TA in a renal transplantation model. Dark Agouti (DA) kidneys were allogeneically transplanted to Wistar-Furth (DA-WF, aTX) rats. Syngeneic grafts (DA-DA, sTX) served as controls. Nine weeks after transplantation, blood pressure, renal function and electrolytes were studied, in addition to real-time PCR, western blot analysis, histology and immunohistochemistry.
  
  
  RESULTS
  In contrast to sTX, the aTX developed IF/TA-dependent renal damage. Ten differentially regulated proteins were identified by 2D gel analysis and mass spectrometry, whereupon five proteins are mainly related to oxidative stress (aldo-keto reductase, peroxiredoxin-1, NAD(+)-dependent isocitrate dehydrogenase, iron-responsive element-binding protein-1 and serum albumin), two participate in cytoskeleton organization (l-plastin and ezrin) and three are assigned to metabolic functions (creatine kinase, ornithine aminotransferase and fructose-1,6-bisphosphatase).
  
  
  CONCLUSIONS
  The proteins related to IF/TA and involved in oxidative stress, cytoskeleton organization and metabolic functions may correspond with novel therapeutic targets.
authors.affiliation: Department of Medicine D, University of Münster, Münster, Germany. sreuter@uni-muenster.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Reuter
authors.forename: Stefanie
authors.initials: S
authors.lastname: Reiermann
authors.forename: Reka
authors.initials: R
authors.lastname: Wörner
authors.forename: Rita
authors.initials: R
authors.lastname: Schröter
authors.forename: Bayram
authors.initials: B
authors.lastname: Edemir
authors.forename: Fritz
authors.initials: F
authors.lastname: Buck
authors.forename: Stefanie
authors.initials: S
authors.lastname: Henning
authors.forename: Jasna
authors.initials: J
authors.lastname: Peter-Katalinic
authors.forename: Beate
authors.initials: B
authors.lastname: Vollenbröker
authors.forename: Kerstin
authors.initials: K
authors.lastname: Amann
authors.forename: Hermann
authors.initials: H
authors.lastname: Pavenstädt
authors.forename: Eberhard
authors.initials: E
authors.lastname: Schlatter
authors.forename: Gert
authors.initials: G
authors.lastname: Gabriëls
mesh_terms: D000818:Animals; D001284:Atrophy / Q000378:metabolism / Q000473:pathology; D003599:Cytoskeleton / Q000378:metabolism; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D005355:Fibrosis / Q000378:metabolism / Q000473:pathology; D016030:Kidney Transplantation; D007684:Kidney Tubules / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009395:Nephritis, Interstitial / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D040901:Proteomics; D051381:Rats; D011919:Rats, Inbred Strains; D011920:Rats, Inbred WF; D014184:Transplantation, Homologous