Objective:To investigate the expression of endoplasmic reticulum stress proteins in photoreceptor apoptosis in light-induced retinal degeneration. Methods: Exposure to excessive levels of light induced photoreceptor apoptosis and had been previously used as a model for the study of retinal degeneration. Photoreceptor apoptosis was detected by terminal dUTP transferase nick end labeling (TUNEL). The protein expression levels of ER stress sensors including glucose-regulated protein-78 (GRP78/BiP), caspase-12, phospho-eukaryotic initiation factor 2? (eIF2?) and phospho-double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase (PERK) were examined by immuno-fluorescence and Western blot analysis. Results: Following light exposure, the protein expression levels of GRP78/BiP, caspase-12, phospho-eIF2? and phospho-PERK were up-regulated in a time dependent manner. The up-regulation of these proteins coincided with or preceded the photoreceptor apoptosis. At the peak of their expression, they were mainly located in the photoreceptor inner segments and/or outer nuclear layers (ONL). Conclusion: Activation of endoplasmic reticulum stress proteins appears to play an important role in light-induced retinal degeneration. Therefore endoplasmic reticulum stress modulators could become a strong candidate for a therapeutic agent in treatment of these diseases.

Background As a hereditary chronic glaucoma model,DBA/2J mouse is widely used in the experimental research of glaucoma worldwide.Although some researches have determined the ocular change induced by hypertention of DBA/2J mouse,there is seldom reports about the research on the relationship of ocular pathological abnormality and development course in DBA/2J mouse.Objective The present study is to characterize the ocular abnormalities and histological changes induced by hypertention in different ages of DBA/2J mice.Methods The clean female DBA/2J mice aged 3-,5-,7-,9-,11-,14-month-old (6 mice for each) were used in this study,and age matched 18 female C57BL/6J mice were as controls.Intraocular pressure (IOP) of mice was measured by anterior chamber puncture of microneedle.The animals were sacrificed and retinal flat mounts were prepared for histopathological examination under the light microscope.Retinal ganglion cells (RGCs) were counted by retinal Nissl staining.Morphology of optic nerve cup in frozen section was examined under the light microscope.The experiment followed the Standard of Association for Research in Vision and Ophthalmology.Results Developing pigment dispersion,iris stroma atrophy,transillumination defects and pupil deformation were found in DBA/2J mice.IOP began to rise in 7-month-old DBA/2J mouse,peaked in 9-month-old mouse and returned to normal in 14-month-old DBA/2J mouse.A significant difference was found in IOP among different ages of DBA/2J mice (F=27.600,P＜0.05) but not C57BL/6J mice (F=0.249,P=0.781).RGCs loss was observed in 7-month-old DBA/2J mice and more serious from 9 to 11-month-old mice,showing a significant decline of RGCs among different ages of DBA/2J mice (F=23.594,P=0.000) but not C57BL/6J mice (F=1.816,P=0.211).The abnormality of optic nerve cupping and decrease of retinal nerve fiber layer were found in 9 to 14-month-old months old DBA/2J mice and were normal in age-matched C57BL/6J mice.Conclusion The abnormal alteration of the ocular anterior segment in DBA/2J mouse is gradually aggravated with aging.The findings of eye in DBA/2J mouse is characterized by secondary glaucoma.DBA/2J mouse offer an ideal animal model for the research of glaucoma.