title: Strong in vivo activation of NF-kappaB in mouse lenses by classic stressors.
abstract: OBJECTIVE
  To examine the in vivo activation of nuclear factor (NF)-kappaB in mouse lens epithelia by using bacterial lipopolysaccharide (LPS), tumor necrosis factor (TNF)-alpha, and UV-B radiation.
  
  
  METHODS
  Transgenic mice containing the NF-kappaB-luciferase reporter were injected with LPS, TNF-alpha or, exposed to UV-B. After various exposure times, the mice were killed, and ocular, liver, lung, kidney, spleen, and skin tissue were obtained. Tissue homogenates were examined for luciferase activity with a luminometer. Groups of mice were also imaged in vivo through a light-intensified camera system to assess NF-kappaB activity.
  
  
  RESULTS
  LPS- and TNF-alpha injected NF-kappaB-luciferase transgenic mice yielded 20- to 40-fold increases in lens NF-kappaB activity, similar to other LPS- and TNF-alpha-responsive organs. Peak NF-kappaB activity occurred 6 hours after injection of TNF-alpha and 12 hours after injection of LPS. Peak activities were, respectively, 3 and 6 hours later than that in other tissues. Mice exposed to 360 J/m(2) of UV-B exhibited a 16-fold increase in NF-kappaB activity 6 hours after exposure, which are characteristics similar to TNF-alpha-exposed mice. In vivo imaging of transgenic mice exposed to LPS, TNF-alpha, and UV-B radiation demonstrated a similarity between in vitro and in vivo measurements of NF-kappaB activity.
  
  
  CONCLUSIONS
  In NF-kappaB-luciferase transgenic mice, NF-kappaB activity occurs in lens epithelial tissue and is activated when the intact mouse is exposed to bacterial LPS, TNF-alpha, or UV-B. Lens epithelial NF-kappaB kinetics were comparable to those of other tissues, indicating that NF-kappaB may play a role in progression or arrest of lens disorders.
authors.affiliation: Institute for Nutrition Research, University of Oslo, Oslo, Norway. george.alexander@basalmed.uio.no
authors.forename: George
authors.initials: G
authors.lastname: Alexander
authors.forename: Harald
authors.initials: H
authors.lastname: Carlsen
authors.forename: Rune
authors.initials: R
authors.lastname: Blomhoff
mesh_terms: D000818:Animals; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D004926:Escherichia coli; D005260:Female; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008156:Luciferases / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008822:Mice, Transgenic; D016328:NF-kappa B / Q000378:metabolism*; D018384:Oxidative Stress; D012867:Skin / Q000378:metabolism / Q000528:radiation effects; D014018:Tissue Distribution; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014466:Ultraviolet Rays
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D008156:Luciferases