Transplanted olfactory ensheathing cells restore retinal function in a rat model of light-induced retinal damage by inhibiting oxidative stress
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Langyue Xue1,2, Yuxiao Zeng1,2, Qiyou Li1,2, Yijian Li1,2, Zhengya Li1,2, Haiwei Xu1,2 and Zhengqin Yin1,2
1Southwest Hospital/Southwest Eye Hospital, Third Military Medical University, Chongqing 400038, China
2Key Lab of Visual Damage and Regeneration & Restoration of Chongqing, Chongqing 400038, China
Haiwei Xu, email: [email protected]
Zhengqin Yin, email: [email protected]
Keywords: light damage, photoreceptor, olfactory ensheathing cells, reactive oxygen species
Received: March 28, 2017 Accepted: August 08, 2017 Published: October 16, 2017
There is still not an effective treatment for continuous retinal light exposure and subsequent photoreceptor degeneration. Olfactory ensheathing cell (OEC) transplantation has been shown to be neuroprotective in spinal cord, and optic nerve injury and retinitis pigmentosa. However, whether OECs protect rat photoreceptors against light-induced damage and how this may work is unclear. Thus, to elucidate this mechanism, purified rat OECs were grafted into the subretinal space of a Long-Evans rat model with light-induced photoreceptor damage. Light exposure decreased a- and b- wave amplitudes and outer nuclear layer (ONL) thickness, whereas the ONL of rats exposed to light for 24 h after having received OEC transplants in their subretinal space was thicker than the PBS control and untreated groups. A- and b- wave amplitudes from electroretinogram of OEC-transplanted rats were maintained until 8 weeks post OEC transplantation. Also, transplanted OECs inhibited formation of reactive oxygen species in retinas exposed to light. In vitro experiments showed that OECs had more total antioxidant capacity in a co-cultured 661W photoreceptor cell line, and cells were protected from damage induced by hydrogen-peroxide. Thus, transplanted OECs preserved retinal structure and function in a rat model of light-induced degeneration by suppressing retinal oxidative stress reactions.
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