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Editor's Highlight: Periodic Exposure to Smartphone-Mimic Low-Luminance Blue Light Induces Retina Damage Through Bcl-2/BAX-Dependent Apoptosis
Author(s) -
ChengHui Lin,
Man-Ru Wu,
Ching-Hao Li,
Hui-Wen Cheng,
Shih-Hsuan Huang,
Chi-Hao Tsai,
Fan-Li Lin,
JauDer Ho,
JawJou Kang,
George Hsiao,
YuWen Cheng
Publication year - 2017
Publication title -
toxicological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.352
H-Index - 183
eISSN - 1096-6080
pISSN - 1096-0929
DOI - 10.1093/toxsci/kfx030
Subject(s) - fadd , retina , retinal pigment epithelium , apoptosis , microbiology and biotechnology , retinal , phototoxicity , fas ligand , retinal degeneration , biology , caspase 3 , chemistry , programmed cell death , caspase , in vitro , neuroscience , biochemistry
Blue light-induced phototoxicity plays an important role in retinal degeneration and might cause damage as a consequence of smartphone dependency. Here, we investigated the effects of periodic exposure to blue light-emitting diode in a cell model and a rat retinal damage model. Retinal pigment epithelium (RPE) cells were subjected to blue light in vitro and the effects of blue light on activation of key apoptotic pathways were examined by measuring the levels of Bcl-2, Bax, Fas ligand (FasL), Fas-associated protein with death domain (FADD), and caspase-3 protein. Blue light treatment of RPE cells increased Bax, cleaved caspase-3, FasL, and FADD expression, inhibited Bcl-2 and Bcl-xL accumulation, and inhibited Bcl-2/Bax association. A rat model of retinal damage was developed with or without continuous or periodic exposure to blue light for 28 days. In this rat model of retinal damage, periodic blue light exposure caused fundus damage, decreased total retinal thickness, caused atrophy of photoreceptors, and injured neuron transduction in the retina.

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