Abstract
Purpose:
To test the hypothesis that treatments of 670 nm red light will modulate activation of Müller cells by using in vivo and in vitro models.
Methods:
In the in vivo experiments, adult Sprague-Dawley albino rats were exposed to bright light (1000 lux) for 24 hours prior to the 670 nm red light (9 J/cm2) treatment and then culled 30 days after bright light damage. The treatment of 670 nm red light commenced at various time points following light damage: 3 (early), 7 (middle) or 14 (late) days for 5 consecutive days. Primary rat Müller cells from postnatal 10-12 day-old rats were prepared for in vitro studies. For the in vitro stress model, uniform scratch wounds were created in Müller cells with 1 mL pipette tips. After the scratch, cells were exposed to 670 nm red light 3 times per day.
Results:
In accordance with results of animal studies, early treatment of 670 nm red light partly rescued the reduction of outer nuclear layer (ONL) thickness and ameliorated the length of the progressive lesion of in superior retinas after bright light damage. Glial fibriallary acidic protein (GFAP), Müller cell-specific stress marker, showed faint immunostaining in hot spots of damaged retinas after early red light treatment. However, middle and late red light treatments did not reduce the expression of GFAP to the same extent. This suggests that the timing to exposure of 670 nm red light after injuries is crucial . By using the in vitro scratching stress model , Müller cells exhibited gliosis including migration, raised levels of GFAP and increased spreading as well as proliferation. The 670 nm red light attenuated the rate of cell migration and the number of mitotic cells. Müller cells treated with 670 nm red light following in vitro stress showed down-regulated expression of GFAP and reduced spreading.
Conclusions:
These data demonstrate that 670 nm red light ameliorated bright light-induced retinal degeneration and activation of Müller cells. The potential protective mechanism of 670 nm red light may be relevant to slowing down gliosis of Müller cells. 670 nm red light would be the promising and efficient therapy in the clinical setting.