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S. Choi, J. Choi, C. Joo; Phosphorylation of Glycogen Synthase Kinase-3beta (Ser9) Mediates Sulindac-Induced Neuronal Cell Survival in the Retinal Ischemia Model . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2935.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Inactivation of glycogen synthase kinase-3beta (GSK-3ß) by Serine9 (Ser9) phosphorylation is implicated in neuronal cell survival. GSK-3ß on Ser9 to render it inactive, a proposed mechanism by which neurons become resistant to apoptotic stimuli. In this study, we examined the involvement of GSK-3ß (Ser9) phosphorylation on retina cell survival by sulindac(SLD) in model of retina ischemia. Methods: Retinal ischemia was induced by increasing intraocular pressure to a range of 160 mm Hg to 180 mm Hg for 60 minutes in adult rats. SLD was treated pre and after (0.01 to 0.1 mM) ischemic injury. In vitro study, the retinas were isolated from at postnatal 1-2day and were subjected to glutamate for ischemic injury. For morphological study, retinas were embedded in resin 24 hours after ischemic injury. The patterns of retinal cell were determined using light microscopy. Western blot analysis was performed using GSK-3ß (Ser9) and phospho-GSK-3ß (Ser9) antibodies. Results: In ischemic animal model, cell death was observed in ischemia group, whereas cell death was obviously reduced in SLD treated grop. In vitro study, attenuated glutamate-induced cell death in dose dependent manners. Furthermore, GSK-3ß (Ser9) phosphorylation were induced in the SLD treated retina than ischemia model. Conclusions: This study suggest that phosphorylation of GSK-3ß(Ser9) mediates SLD-induced neuronal cell survival in the retinal ischemia model.
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