Abstract

Ageing and alteration of the functions of the retinal pigment epithelium (RPE) are at the origin of lost of vision seen in age‐related macular degeneration (AMD). The RPE is known to be vulnerable to high‐energy blue light. The white light‐emitting diodes (LED) commercially available have relatively high content of blue light, a feature that suggest that they could be deleterious for this retinal cell layer. The aim of our study was to investigate the effects of “white LED” exposure on RPE. For this, commercially available white LEDs were used for exposure experiments on Wistar rats. Immunohistochemical stain on RPE flat mount, transmission electron microscopy and Western blot were used to exam the RPE. LED‐induced RPE damage was evaluated by studying oxidative stress, stress response pathways and cell death pathways as well as the integrity of the outer blood–retinal barrier (BRB). We show that white LED light caused structural alterations leading to the disruption of the outer blood–retinal barrier. We observed an increase in oxidized molecules, disturbance of basal autophagy and cell death by necrosis. We conclude that white LEDs induced strong damages in rat RPE characterized by the breakdown of the BRB and the induction of necrotic cell death.

Highlights

  • The retinal pigment epithelium (RPE) is a specialized monolayer of hexanocuboidal cells lying between the photoreceptors and the choriocapillaris

  • RPE has an important role in the clearing of oxidized photoreceptors outer segments, and the light damage at its level could be responsible for the degeneration of the neural retina, a feature seen in age-related macular degeneration (AMD)

  • The results presented were obtained in an experimental condition and cannot be directly transposed to humans, they raise two important questions: How will the RPE cells manage to control the oxidative stress produced over years of exposure to this type of light sources? And how will repeated exposure affect specific functions such as autophagy and phagocytosis of photoreceptors outer segments?

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Summary

Introduction

The RPE is a specialized monolayer of hexanocuboidal cells lying between the photoreceptors and the choriocapillaris. RPE cells are interconnected by tight and adherents junctions that isolate photoreceptors from fenestrated capillaries of the choroid, forming a selective barrier called the outer BRB [1]. RPE participates in phagocytosis of spent photoreceptors’ outer segments (OS) [2], transepithelial transport of nutrients and waste products [3], visual cycle [2], protection against light and oxidative stress [4], as well as to the production of growth factors. Structural or it is generally accepted that the primary cause of AMD is the degeneration of the RPE [6], the causes of this degeneration are less understood. The influence of light exposure has been widely discussed, but it is established that light is an important factor in the progression of AMD [7,8,9]

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