Animal Models of LED-Induced Phototoxicity. Short- and Long-Term In Vivo and Ex Vivo Retinal Alterations.
Juan Antonio Miralles de Imperial-OlleroAlejandro Gallego-OrtegaArturo Ortin-MartinezMaría Paz Villegas-PérezFrancisco J Valiente-SorianoManuel Vidal-SanzPublished in: Life (Basel, Switzerland) (2021)
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.
Keyphrases
- diabetic retinopathy
- age related macular degeneration
- optical coherence tomography
- induced apoptosis
- cell cycle arrest
- oxidative stress
- optic nerve
- high glucose
- diabetic rats
- endothelial cells
- light emitting
- multiple sclerosis
- case control
- endoplasmic reticulum stress
- multidrug resistant
- drug induced
- inflammatory response
- cerebral ischemia
- vascular endothelial growth factor
- signaling pathway
- cell death
- spinal cord injury
- cell proliferation
- lipopolysaccharide induced
- pi k akt
- functional connectivity
- lps induced
- solar cells