Gyu Hyun Kim1, Hyung Il Kim2, Sun-Sook Paik1, Sung Won Jung1, Seungbum Kang3, In-Beom Kim4,5. 1. Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Korea. 2. Gyeongju St. Mary's Eye Clinic, 293 Wonhwa-ro, Gyeongju-si, Gyeongsangbuk-do, 780-946, Korea. 3. Department of Ophthalmology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Korea. 4. Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Korea. ibkimmd@catholic.ac.kr. 5. Catholic Institute for Applied Anatomy, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Korea. ibkimmd@catholic.ac.kr.
Abstract
PURPOSE: The purpose of this study was to evaluate a retinal degeneration (RD) model induced by exposing mice to a blue light-emitting diode (LED), which led to photoreceptor cell death. METHODS: RD was induced in BALB/c mice by exposure to a blue LED (460 nm) for 2 hours. Retinal function was examined using scotopic electroretinography (ERG). Histopathological changes were assessed by hematoxylin and eosin (H&E) staining and electron microscopy. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. In addition, retinal inflammation and oxidative stress were evaluated by immunohistochemistry with anti-glial fibrillary acidic protein (GFAP) and anti-8-hydroxy-2'-deoxyguanosine (8-OHdG), respectively. RESULTS: Scotopic ERG showed that blue LED exposure resulted in a decrease in both a-waves and b-waves in mice retinas in an illuminance-dependent manner. H&E, TUNEL assay, and electron microscopy revealed massive photoreceptor cell death by apoptosis in the central region of the retina. Retinal stress and inflammation were detected by increased expression of GFAP and by electron microscopy findings demonstrating microglia infiltration in the outer nuclear layer and subretinal space. In addition, increased labeling of 8-OHdG was observed in the retinas from blue LED exposure. CONCLUSIONS: These results suggest that blue LED-induced RD may be a useful animal model in which to study the pathogenesis of RD, including age-related macular degeneration, and to evaluate the effects of new therapeutic agents prior to clinical trials, where oxidative stress and inflammation are the underlying RD mechanisms.
PURPOSE: The purpose of this study was to evaluate a retinal degeneration (RD) model induced by exposing mice to a blue light-emitting diode (LED), which led to photoreceptor cell death. METHODS: RD was induced in BALB/c mice by exposure to a blue LED (460 nm) for 2 hours. Retinal function was examined using scotopic electroretinography (ERG). Histopathological changes were assessed by hematoxylin and eosin (H&E) staining and electron microscopy. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. In addition, retinal inflammation and oxidative stress were evaluated by immunohistochemistry with anti-glial fibrillary acidic protein (GFAP) and anti-8-hydroxy-2'-deoxyguanosine (8-OHdG), respectively. RESULTS: Scotopic ERG showed that blue LED exposure resulted in a decrease in both a-waves and b-waves in mice retinas in an illuminance-dependent manner. H&E, TUNEL assay, and electron microscopy revealed massive photoreceptor cell death by apoptosis in the central region of the retina. Retinal stress and inflammation were detected by increased expression of GFAP and by electron microscopy findings demonstrating microglia infiltration in the outer nuclear layer and subretinal space. In addition, increased labeling of 8-OHdG was observed in the retinas from blue LED exposure. CONCLUSIONS: These results suggest that blue LED-induced RD may be a useful animal model in which to study the pathogenesis of RD, including age-related macular degeneration, and to evaluate the effects of new therapeutic agents prior to clinical trials, where oxidative stress and inflammation are the underlying RD mechanisms.
Authors: Camila C Pinto; Kamila C Silva; Subrata K Biswas; Natássia Martins; José B Lopes De Faria; Jacqueline M Lopes De Faria Journal: Free Radic Res Date: 2007-10
Authors: Grazyna Palczewska; Patrycjusz Stremplewski; Susie Suh; Nathan Alexander; David Salom; Zhiqian Dong; Daniel Ruminski; Elliot H Choi; Avery E Sears; Timothy S Kern; Maciej Wojtkowski; Krzysztof Palczewski Journal: JCI Insight Date: 2018-09-06