Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations

Phototoxicity animal models have been largely studied due to their degenerative communalities with human pathologies, e.g., age-related macular degeneration (AMD). Studies have documented not only the effects of white light exposure, but also other wavelengths using LEDs, such as blue or green light...

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Autores principales: Juan A. Miralles de Imperial-Ollero, Alejandro Gallego-Ortega, Arturo Ortín-Martínez, María Paz Villegas-Pérez, Francisco J. Valiente-Soriano, Manuel Vidal-Sanz
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/85fbaeda6b8a4df690cd2c8ca497a1b3
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spelling oai:doaj.org-article:85fbaeda6b8a4df690cd2c8ca497a1b32021-11-25T18:10:34ZAnimal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations10.3390/life111111372075-1729https://doaj.org/article/85fbaeda6b8a4df690cd2c8ca497a1b32021-10-01T00:00:00Zhttps://www.mdpi.com/2075-1729/11/11/1137https://doaj.org/toc/2075-1729Phototoxicity animal models have been largely studied due to their degenerative communalities with human pathologies, e.g., age-related macular degeneration (AMD). Studies have documented not only the effects of white light exposure, but also other wavelengths using LEDs, such as blue or green light. Recently, a blue LED-induced phototoxicity (LIP) model has been developed that causes focal damage in the outer layers of the superior-temporal region of the retina in rodents. In vivo studies described a progressive reduction in retinal thickness that affected the most extensively the photoreceptor layer. Functionally, a transient reduction in a- and b-wave amplitude of the ERG response was observed. Ex vivo studies showed a progressive reduction of cones and an involvement of retinal pigment epithelium cells in the area of the lesion and, in parallel, an activation of microglial cells that perfectly circumscribe the damage in the outer retinal layer. The use of neuroprotective strategies such as intravitreal administration of trophic factors, e.g., basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF) or pigment epithelium-derived factor (PEDF) and topical administration of the selective alpha-2 agonist (Brimonidine) have demonstrated to increase the survival of the cone population after LIP.Juan A. Miralles de Imperial-OlleroAlejandro Gallego-OrtegaArturo Ortín-MartínezMaría Paz Villegas-PérezFrancisco J. Valiente-SorianoManuel Vidal-SanzMDPI AGarticleLED induced phototoxicitycone photoreceptormicroglia activationretinal pigment epitheliumneuroprotectionScienceQENLife, Vol 11, Iss 1137, p 1137 (2021)
institution DOAJ
collection DOAJ
language EN
topic LED induced phototoxicity
cone photoreceptor
microglia activation
retinal pigment epithelium
neuroprotection
Science
Q
spellingShingle LED induced phototoxicity
cone photoreceptor
microglia activation
retinal pigment epithelium
neuroprotection
Science
Q
Juan A. Miralles de Imperial-Ollero
Alejandro Gallego-Ortega
Arturo Ortín-Martínez
María Paz Villegas-Pérez
Francisco J. Valiente-Soriano
Manuel Vidal-Sanz
Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
description Phototoxicity animal models have been largely studied due to their degenerative communalities with human pathologies, e.g., age-related macular degeneration (AMD). Studies have documented not only the effects of white light exposure, but also other wavelengths using LEDs, such as blue or green light. Recently, a blue LED-induced phototoxicity (LIP) model has been developed that causes focal damage in the outer layers of the superior-temporal region of the retina in rodents. In vivo studies described a progressive reduction in retinal thickness that affected the most extensively the photoreceptor layer. Functionally, a transient reduction in a- and b-wave amplitude of the ERG response was observed. Ex vivo studies showed a progressive reduction of cones and an involvement of retinal pigment epithelium cells in the area of the lesion and, in parallel, an activation of microglial cells that perfectly circumscribe the damage in the outer retinal layer. The use of neuroprotective strategies such as intravitreal administration of trophic factors, e.g., basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF) or pigment epithelium-derived factor (PEDF) and topical administration of the selective alpha-2 agonist (Brimonidine) have demonstrated to increase the survival of the cone population after LIP.
format article
author Juan A. Miralles de Imperial-Ollero
Alejandro Gallego-Ortega
Arturo Ortín-Martínez
María Paz Villegas-Pérez
Francisco J. Valiente-Soriano
Manuel Vidal-Sanz
author_facet Juan A. Miralles de Imperial-Ollero
Alejandro Gallego-Ortega
Arturo Ortín-Martínez
María Paz Villegas-Pérez
Francisco J. Valiente-Soriano
Manuel Vidal-Sanz
author_sort Juan A. Miralles de Imperial-Ollero
title Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
title_short Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
title_full Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
title_fullStr Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
title_full_unstemmed Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations
title_sort animal models of led-induced phototoxicity. short- and long-term in vivo and ex vivo retinal alterations
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/85fbaeda6b8a4df690cd2c8ca497a1b3
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