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Core Transcription Programs Controlling Injury-Induced Neurodegeneration of Retinal Ganglion Cells

ABSTRACT: Core Transcription Programs Controlling Injury-Induced Neurodegeneration of Retinal Ganglion Cells

PROVIDER: PRJNA787937 | ENA |

REPOSITORIES: ENA

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Core Transcription Programs Controlling Injury-Induced Neurodegeneration of Retinal Ganglion Cells

Project description:In this study, we performed RNA-seq of injured and FACS-purified RGCs receiving CRISPR-mediated knockout of ATF3, ATF4, CEBPγ or CHOP

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IGF-I-induced chronic gliosis and retinal stress lead to neurodegeneration in an animal model of retinopathy

Project description:IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.

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[E-MEXP-3786] IGF-I-induced chronic gliosis and retinal stress lead to neurodegeneration in an animal model of retinopathy

Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death. 3 transgenic and 3 wild type biological replicates examined.

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