Abstract
Purpose: :
Light exposure using the red to near-infrared region of the spectrum (670nm) is an emerging new therapy which has beneficial effects in several disease models. In this study, we used a mouse model of oxygen-induced retinal degeneration, pre-treated with 670nm light, aiming to identify differentially regulated pro-inflammatory and pro-apoptotic genes.
Methods: :
Experimental C57BL/6J mice were pre-treated with 670nm light (9J/cm2) for 3mins daily for 5 consecutive days. Pre-treated animals were placed in hyperoxic environment (75% oxygen). Retinas were collected after 0 (controls), 3, 7, 10 or 14 days of exposure to hyperoxia (n=10/group) and prepared either for histological analysis, or for RNA extraction and quantitative real-time PCR (qPCR). Localization of glial fibrillary acidic protein (GFAP), distribution of TUNEL-positive profiles and photoreceptor population were evaluated histologically. Expression levels of pro-inflammatory and pro-apoptotic genes were assessed using qPCR.
Results: :
In non pre-treated animals, exposure to hyperoxia promoted photoreceptor cell death, increased immunoreactivity to GFAP and caused erosion of the outer blood retinal barrier. Compared to control animals, an increase in the expression of the pro-inflammatory genes CCL2,CCL3 and ICAM, stress marker GFAP, pro-apoptotic c-jun and proto-oncogene BCL-3 were observed following hyperoxia. These effects were also seen in pre-treated retinas, but with changes less severe than the non pre-treated animals from timepoint-matched control retinas (p<0.005).
Conclusions: :
The damaging effects of hyperoxia on photoreceptors were ameliorated following pre-treatment with 670nm light. These results suggest that pre-treatment with 670nm light may provide stability of the retina against hyperoxia-induced degeneration.
Keywords: degenerations/dystrophies • apoptosis/cell death • inflammation