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E-MEXP-3786

ABSTRACT: Transcription profiling by array of mouse male retinas to investugate IGF-I-induced chronic gliosis and retinal stress

PROVIDER: E-MEXP-3786 | ExpressionAtlas | 2015-10-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-3786-analysis-methods.tsv	Tabular
	E-MEXP-3786-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-3786-configuration.xml	Xml
	E-MEXP-3786-percentile-ranks.tsv	Tabular
	E-MEXP-3786.condensed-sdrf.tsv	Tabular

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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.

2013-04-30 | GSE46246 | GEO

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

2013-04-30 | E-GEOD-46246 | biostudies-arrayexpress

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.

2013-08-01 | E-MEXP-3786 | biostudies-arrayexpress

Mitochondrial control of hypoxia-induced pathological retinal angiogenesis

Project description:Objective: Pathological retinal angiogenesis is vision threatening. In mouse oxygen-induced retinopathy (OIR) we sought to define mitochondrial respiration changes longitudinally during hyperoxia-induced vessel loss and with hypoxia-induced neovascularization (NV), and test interventions to address those changes to prevent NV. Methods: OIR was induced in C57BL/6J mice and retinal vasculature was examined at maximum neovessel formation. We assessed total proteome change and the ratio of mitochondrial/nuclear DNA copy numbers (mtDNA/nDNA) of OIR vs. control retinas, and mitochondrial oxygen consumption rates (OCR) in ex vivo OIR vs. control retinas (BaroFuse). Pyruvate vs. vehicle control was supplemented in OIR mice either prior to or during neovessel formation. Results: In OIR vs. control retinas proteomics identified decreased retinal mitochondrial respiration and synaptic formation pathway proteins at peak neovascularization. mtDNA/nDNA was decreased during hypoxia-induced neovessel growth (as was OCR) suggesting impaired mitochondrial respiration. Pyruvate administration during but not prior to neovessel formation (in line with compromised mitochondrial activity) suppressed NV in vivo. Conclusions: Mitochondrial energetics are suppressed during retinal NV in OIR. Appropriately timed supplementation of energy substrates (pyruvate) may be a novel approach in neovascular retinal diseases.

2025-05-06 | PXD051410 | Pride

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Project description:FACS-array profiling in retinal endothelial cells from living mouse retinas

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Murine retina: Control vs. experimental autoimmune uveoretinitis

Project description:Transcriptional profiling of mouse retina comparing naïve mouse and experimental autoimmune uveoretinitis (EAU)-developing mouse. EAU was induced by immunization of retinal autoantigens in adjuvants. Retinas were harvested 14 days after immunization.

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Gene expression in retina and LGN of wild type and Chrnb2-/- mice

Project description:Mice lacking the beta 2 subunit (Chrnb2) of the neuronal nicotinic acetylcholine receptor display altered retinal waves and disorganized projections of the retinal ganglion cells to the lateral geniculate nucleus (LGN). mRNA populations from retinas and LGN from Chrnb2-/-and wild type (C57BL/6J) mice were compared at 4 days postnatal, when RGC segregation to the LGN begins in WT mice. Retinal mRNAs were also compared at adulthood. Using microarray hybridization, we identified transcripts which are differentially expressed between Chrnb2-/- and wild type animals in these two tissues at these two ages. mRNA was isolated from retina and LGN of three male littermates each of WT and Chrnb2-/- mice at P4. mRNA from retinas of two adult male littermates of each type was also examined.

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Expression profiling of microRNAs in oxygen-induced retinal neovascularization in mice

Project description:The purpose of this study is to identify disease-related miRNAs in retinas of a mouse model of oxygen-induced retinopathy (OIR). OIR pups were exposed to 75% oxygen at postnatal day (P)7 for 5 days, and were returned to room air at P12. The miRNAs expression profiles in the retinas from OIR mice at P17 and room air controls were determined through microarray analysis. Expressions of significantly upregulated and downregulated miRNAs in the OIR retinas and controls were confirmed through quantitative real-time RT-PCR (qPCR). Compared to the room air controls, 3 miRNAs were significantly up-regulated, and 8 miRNAs were down-regulated in OIR retinas. Our findings indicated that several miRNAs were differentially expressed in the oxygen-induced retinal neovascularization, which might provide novel therapeutic targets in regulating retinal neovascular diseases.

2018-06-19 | GSE115949 | GEO

Gene Expression Profile of Hyperoxic/hypoxic Retinas in Mouse Model of Oxygen-induced Retinopathy

Project description:Retinal ischemia is believed to initiate a series of events that leads to retinal neovascularization observed in several retinal diseases such as diabetetic retinopathy and retinal vein occlusion. Although some molecules such as VEGF and MCP-1 have been implicated in the process, its underlying mechanisms remain elusive. In order to identify genes associated with retinal ischemia, we performed gene expression analyses in retinas of mouse model of oxygen-induced retinopathy using DNA microarray technology.

2010-01-15 | GSE19886 | GEO

Mus musculus

Project description:FACS-array profiling in retinal endothelial cells from living mouse retinas without pericyte coverage

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