Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations
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 (CeO<sub>2</sub>-NPs or nanoceria), which...
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doaj-f65c4424211c4b82a18a9b5d442352e82020-11-25T03:24:23ZengMDPI AGCells2073-44092020-07-0191617161710.3390/cells9071617Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy AlterationsAnnamaria Tisi0Vincenzo Flati1Simona Delle Monache2Luca Lozzi3Maurizio Passacantando4Rita Maccarone5Department of Biotechnology and Applied Clinical Sciences, University of L’Aquila, via Vetoio, Coppito 2, 67100 L’Aquila, ItalyDepartment of Biotechnology and Applied Clinical Sciences, University of L’Aquila, via Vetoio, Coppito 2, 67100 L’Aquila, ItalyDepartment of Biotechnology and Applied Clinical Sciences, University of L’Aquila, via Vetoio, Coppito 2, 67100 L’Aquila, ItalyDepartment of Physical and Chemical Sciences, University of L’Aquila, via Vetoio, Coppito 1, 67100 L’Aquila, ItalyDepartment of Physical and Chemical Sciences, University of L’Aquila, via Vetoio, Coppito 1, 67100 L’Aquila, ItalyDepartment of Biotechnology and Applied Clinical Sciences, University of L’Aquila, via Vetoio, Coppito 2, 67100 L’Aquila, ItalyRetinal 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 (CeO<sub>2</sub>-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 CeO<sub>2</sub>-NPs promoted cell viability against H<sub>2</sub>O<sub>2</sub>–induced cellular damage. For the in vivo studies, we used a rat model of acute light damage (LD), which mimics many features of AMD. CeO<sub>2</sub>-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. CeO<sub>2</sub>-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 CeO<sub>2</sub>-NPs represent an eligible candidate to counteract RPE degeneration and, therefore, a powerful therapy for AMD.https://www.mdpi.com/2073-4409/9/7/1617nanomedicinenanoceriaretinal pigment epitheliumlight damageautophagyatrophic AMD |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Annamaria Tisi Vincenzo Flati Simona Delle Monache Luca Lozzi Maurizio Passacantando Rita Maccarone |
spellingShingle |
Annamaria Tisi Vincenzo Flati Simona Delle Monache Luca Lozzi Maurizio Passacantando Rita Maccarone Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations Cells nanomedicine nanoceria retinal pigment epithelium light damage autophagy atrophic AMD |
author_facet |
Annamaria Tisi Vincenzo Flati Simona Delle Monache Luca Lozzi Maurizio Passacantando Rita Maccarone |
author_sort |
Annamaria Tisi |
title |
Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations |
title_short |
Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations |
title_full |
Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations |
title_fullStr |
Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations |
title_full_unstemmed |
Nanoceria Particles Are an Eligible Candidate to Prevent Age-Related Macular Degeneration by Inhibiting Retinal Pigment Epithelium Cell Death and Autophagy Alterations |
title_sort |
nanoceria particles are an eligible candidate to prevent age-related macular degeneration by inhibiting retinal pigment epithelium cell death and autophagy alterations |
publisher |
MDPI AG |
series |
Cells |
issn |
2073-4409 |
publishDate |
2020-07-01 |
description |
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 (CeO<sub>2</sub>-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 CeO<sub>2</sub>-NPs promoted cell viability against H<sub>2</sub>O<sub>2</sub>–induced cellular damage. For the in vivo studies, we used a rat model of acute light damage (LD), which mimics many features of AMD. CeO<sub>2</sub>-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. CeO<sub>2</sub>-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 CeO<sub>2</sub>-NPs represent an eligible candidate to counteract RPE degeneration and, therefore, a powerful therapy for AMD. |
topic |
nanomedicine nanoceria retinal pigment epithelium light damage autophagy atrophic AMD |
url |
https://www.mdpi.com/2073-4409/9/7/1617 |
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