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Strong In Vivo Activation of NF-B in Mouse Lenses by Classic Stressors

¹From the Institute for Nutrition Research, University of Oslo, Oslo, Norway.

PURPOSE. To examine the in vivo activation of nuclear factor (NF)-B in mouse lens epithelia by using bacterial lipopolysaccharide (LPS), tumor necrosis factor (TNF)-, and UV-B radiation.

METHODS. Transgenic mice containing the NF-B-luciferase reporter were injected with LPS, TNF- 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-B activity.

RESULTS. LPS- and TNF- injected NF-B-luciferase transgenic mice yielded 20- to 40-fold increases in lens NF-B activity, similar to other LPS- and TNF-–responsive organs. Peak NF-B activity occurred 6 hours after injection of TNF- 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-B activity 6 hours after exposure, which are characteristics similar to TNF-–exposed mice. In vivo imaging of transgenic mice exposed to LPS, TNF-, and UV-B radiation demonstrated a similarity between in vitro and in vivo measurements of NF-B activity.

CONCLUSIONS. In NF-B-luciferase transgenic mice, NF-B activity occurs in lens epithelial tissue and is activated when the intact mouse is exposed to bacterial LPS, TNF-, or UV-B. Lens epithelial NF-B kinetics were comparable to those of other tissues, indicating that NF-B may play a role in progression or arrest of lens disorders.

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