Abstract
Retinal pigment epithelium (RPE) dysfunction and degeneration underlie the development of age-related macular degeneration (AMD), which is the leading cause of blindness worldwide. In this study, we investigated whether cerium oxide nanoparticles (CeO2-NPs or nanoceria), which are anti-oxidant agents with auto-regenerative properties, are able to preserve the RPE. On ARPE-19 cells, we found that CeO2-NPs promoted cell viability against H2O2–induced cellular damage. For the in vivo studies, we used a rat model of acute light damage (LD), which mimics many features of AMD. CeO2-NPs intravitreally injected three days before LD prevented RPE cell death and degeneration and nanoceria labelled with fluorescein were found localized in the cytoplasm of RPE cells. CeO2-NPs inhibited epithelial-mesenchymal transition of RPE cells and modulated autophagy by the down-regulation of LC3B-II and p62. Moreover, the treatment inhibited nuclear localization of LC3B. Taken together, our study demonstrates that CeO2-NPs represent an eligible candidate to counteract RPE degeneration and, therefore, a powerful therapy for AMD.
Highlights
Retinal pigment epithelium (RPE) is a monolayer of post-mitotic, non-regenerating epithelial cells which, together with the choriocapillaris and Bruch’s membrane, constitutes the outer blood retinal barrier (BRB) structure [1,2]
The dry form of age-related macular degeneration (AMD) is characterized by progressive lipofuscin/drusen accumulation associated with the slow apoptosis of RPE, neuroretina, and choriocapillaris and, in the end, with permanent central
We have previously demonstrated that light damage induced oxidative stress, which was reduced in the photoreceptor layer by the antioxidant activity of cerium oxide nanoparticles
Summary
Retinal pigment epithelium (RPE) is a monolayer of post-mitotic, non-regenerating epithelial cells which, together with the choriocapillaris and Bruch’s membrane, constitutes the outer blood retinal barrier (BRB) structure [1,2]. At their apical surface, RPE cells are connected through tight junctions, which allow them to form a barrier. RPE cells are connected through tight junctions, which allow them to form a barrier This leads to a size-selective passive diffusion of molecules [3]. The dry form of AMD is characterized by progressive lipofuscin/drusen accumulation associated with the slow apoptosis of RPE, neuroretina, and choriocapillaris and, in the end, with permanent central
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