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Weiyong Shen, So-Ra Lee, Joana Araujo, Sook H Chung, Ling Zhu, Mark C Gillies; Effect of glucocorticoids on neuronal and vascular pathology in a transgenic model of selective Müller cell ablation. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2277.
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Many retinal diseases exhibit pathological processes that affect both neurons and blood vessels. Treatments that address both at the same time might have advantages over more specific approaches, such as vascular endothelial growth factor (VEGF) inhibitors which are used to treat vascular leak but are suspected to have a neurotoxic effect. The aim of this study was to evaluate the effects of an intravitreal injection of triamcinolone acetonide (TA) in a transgenic model in which patchy Müller cell ablation leads to photoreceptor degeneration, vascular leak and intraretinal neovascularization.
TA was injected 4 days before induced Müller cell ablation. Changes in photoreceptors, microglia and Müller cells, differential expression of P75 neurotrophin receptor (p75NTR), tumor necrosis factor-α (TNFα), the precursor and mature forms of neurotrophin 3 (pro-NT3 and NT3) and activation of the p53 and p38 stress-activated protein kinase (p38/SAPK) signalling pathways were examined. We also evaluated the effects of TA on retinal vascular pathology.
We found that TA prevented photoreceptor degeneration and inhibited reactive activation of microglial and Müller cells. TA also attenuated Müller cell loss and inhibited overexpression of P75NTR, TNFα, pro-NT and the activation of p53 and p38/SAPK signalling pathways. TA not only prevented the development of retinal vascular lesions but also inhibited fluorescein leakage from established vascular lesions. TA inhibited overexpression of VEGF in transgenic mice but without affecting its basal level expression in the normal retina.
Our data suggest that glucocorticoid treatment may be beneficial for treatment of retinal diseases that affect both neurons and the vasculature.
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