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Y. Ito, M. Shimazawa, Y. Inokuchi, A. Miwa, H. Yamanaka, K. Tsuruma, H. Onoe, M. Araie, H. Hara; Involvement of Endoplasmic Reticulum Stress on Neuronal Degeneration in the Lateral Geniculate Nucleus in the Monkey Glaucoma Model. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6117.
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Endoplasmic reticulum (ER) stress is involved in neurodegenerative diseases, including glaucoma. However, it has been unclear yet whether ER stress induces the neuronal death in the glaucomatous LGN. In this study, we investigated the involvement of ER stress on the pathophysiological mechanisms underlying neuronal death of the LGN after the intraocular pressure (IOP) elevation.
Two cynomolgus monkeys, each with a glaucomatous left eye by laser-photocoagulation treatment, were studied. At 4 and 24 weeks after the laser-photocoagulation treatment, the numbers of LGN neuron and atrophy were evaluated by immunohistchemistry using parvalbumin-antibody that was used to specifically label relay neurons connecting to the visual cortex.
Loss of neurons and/or neuronal atrophy in layer 1 of LGN (magnocellular layer) were observed at both 4 and 24 weeks after the laser-photocoagulation treatment, and in layers 4 and 6 of LGN (parvocellular layer) at 24 weeks. In the LGN region, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, polyubiquitin, and production of ER stress-related proteins, such as the phosphorylation of eukaryotic initiation factor 2α (p-eIF2α) and C/EBP-homologous protein (CHOP), were also detected by in situ hybridization and immunostaining.
These findings indicate that ER-stress may play some roles in neuronal death of the LGN after the IOP elevation.
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