Purchase this article with an account.
George Alexander, Harald Carlsen, Rune Blomhoff; Strong In Vivo Activation of NF-κB in Mouse Lenses by Classic Stressors. Invest. Ophthalmol. Vis. Sci. 2003;44(6):2683-2688. doi: 10.1167/iovs.02-0829.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To examine the in vivo activation of nuclear factor (NF)-κB in mouse lens epithelia by using bacterial lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, and UV-B radiation.
methods. Transgenic mice containing the NF-κB-luciferase reporter were injected with LPS, TNF-α 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-κB activity.
results. LPS- and TNF-α injected NF-κB-luciferase transgenic mice yielded 20- to 40-fold increases in lens NF-κB activity, similar to other LPS- and TNF-α–responsive organs. Peak NF-κB activity occurred 6 hours after injection of TNF-α 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/m2 of UV-B exhibited a 16-fold increase in NF-κB activity 6 hours after exposure, which are characteristics similar to TNF-α–exposed mice. In vivo imaging of transgenic mice exposed to LPS, TNF-α, and UV-B radiation demonstrated a similarity between in vitro and in vivo measurements of NF-κB activity.
conclusions. In NF-κB-luciferase transgenic mice, NF-κB activity occurs in lens epithelial tissue and is activated when the intact mouse is exposed to bacterial LPS, TNF-α, or UV-B. Lens epithelial NF-κB kinetics were comparable to those of other tissues, indicating that NF-κB may play a role in progression or arrest of lens disorders.
This PDF is available to Subscribers Only