title: Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation.
abstract: BACKGROUND
  Hyperoxic reoxygenation following hypoxia increases the expression of inflammatory genes in the neonatal mouse brain. We have therefore compared the temporal profile of 44 a priori selected genes after hypoxia and hyperoxic or normoxic reoxygenation.
  
  
  METHODS
  Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O2) and 30 min reoxygenation with 60% or 21% O2. After 0 to 72 h observation, mRNA and protein were examined in the hippocampus and striatum.
  
  
  RESULTS
  There were significantly higher gene expression changes in six genes after hyperoxic compared to normoxic reoxygenation. Three genes had a generally higher expression throughout the observation period: the inflammatory genes Hmox1 (mean difference: 0.52, 95% confidence interval (CI): 0.15-1.01) and Tgfb1 (mean difference: 0.099, CI: 0.003-0.194), and the transcription factor Nfkb1 (mean difference: 0.049, CI: 0.011-0.087). The inflammatory genes Cxcl10 and Il1b, and the DNA repair gene Neil3, had a higher gene expression change after hyperoxic reoxygenation at one time point only. Nineteen genes involved in inflammation, transcription regulation, apoptosis, angiogenesis, and glucose transport had significantly different gene expression changes with time in all intervention animals.
  
  
  CONCLUSIONS
  We confirm that hyperoxic reoxygenation induces a stronger inflammatory gene response than reoxygenation with air.
authors.affiliation: Department of Pediatric Research, University of Oslo, Oslo University Hospital HF, Oslo, Norway.
authors.forename: Anne Gro W
authors.initials: AG
authors.lastname: Rognlien
authors.affiliation: Department of Pediatric Research, University of Oslo, Oslo University Hospital HF, Oslo, Norway.
authors.forename: Embjørg J
authors.initials: EJ
authors.lastname: Wollen
authors.affiliation: 1] Department of Pediatric Research, University of Oslo, Oslo University Hospital HF, Oslo, Norway [2] Department of Clinical Molecular Biology and Laboratory Sciences, Akershus University Hospital, Lørenskog, Norway.
authors.forename: Monica
authors.initials: M
authors.lastname: Atneosen-Åsegg
authors.affiliation: Department of Pediatric Research, University of Oslo, Oslo University Hospital HF, Oslo, Norway.
authors.forename: Ola Didrik
authors.initials: OD
authors.lastname: Saugstad
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000235:genetics; D003342:Corpus Striatum / Q000378:metabolism*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000502:physiology*; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D018496:Hyperoxia / Q000378:metabolism*; D000860:Hypoxia / Q000503:physiopathology*; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D052002:NF-kappa B p50 Subunit / Q000378:metabolism; D010100:Oxygen / Q000008:administration & dosage / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D008565:Membrane Proteins; D052002:NF-kappa B p50 Subunit; C508961:Tgfb1 protein, mouse; D053773:Transforming Growth Factor beta1; C073701:Nfkb1 protein, mouse; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse; D010100:Oxygen