Purchase this article with an account.
Hirohiko Kawashima, Hideto Osada, Tomohiro Okamoto, Norimitsu Ban, Mamoru Kamoshita, Toshihide Kurihara, Norihiro Nagai, Kazuo Tsubota, Yoko Ozawa; Light-induced retinal degeneration and AMPK. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5416.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Light exposure can cause development and progression of retinal degenerative diseases such as age-related macular degeneration and retinitis pigmentosa, major causes of blindness. However, the mechanisms underlying light-induced tissue damage are not fully understood. In this study, we evaluated the molecular events after light exposure in the retina, focusing on the visual pigment, rhodopsin, and a cellular energy sensor, AMP-activated protein kinase (AMPK) signaling.
Seven week-old mice were dark-adapted for 12 hrs, and then exposed to 3000 lux from a white fluorescence lamp for 1 hr, in a dedicated exposure box maintained at 22 ± 20C, containing stainless-steel mirrors on each wall and on the floor. Following light exposure, the mice were returned to their cages and maintained under dim cyclic light until they were euthanized 24 or 48 h after light exposure to obtain the retinal protein samples. The protein levels of rhodopsin, phosphorylated and activated AMPK were measured by immunoblot analyses.
The protein level of rhodopsin was reduced 48 hrs after light exposure, and that of activated AMPK was reduced 24 hrs after light exposure, in the retina of mice exposed to the light compared with those with no light exposure.
Rhodopsin, the visual pigment that can determine visual function was reduced, and in parallel, activated AMPK was also reduced, in the retina of light exposed mice. Further study to know the relationship between AMPK and rhodopsin will help reveal the underlying mechanism of light-induced retinal degeneration.
This PDF is available to Subscribers Only