E-MEXP-3786
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-3786 | ExpressionAtlas | 2015-10-22
REPOSITORIES: ExpressionAtlas
Similar Datasets
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
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.
2013-04-30 | E-GEOD-46246 | biostudies-arrayexpress
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
Project description:FACS-array profiling in retinal endothelial cells from living mouse retinas
| PRJNA137491 | ENA
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.
2010-07-01 | GSE22617 | GEO
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.
2011-01-01 | E-GEOD-22824 | biostudies-arrayexpress
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
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
Project description:Photoreceptor disorders are collectively known as retinal degeneration (RD), and include retinitis pigmentosa (RP), cone-rod dystrophy and age related macular degeneration (AMD). These disorders are largely genetic in origin; individual mutations in any one of >200 genes cause RD, making mutation specific therapies prohibitively expensive. A better treatment plan, particularly for late stage disease, may involve stem cell transplants into the photoreceptor or ganglion cell layers of the retina. Stem cells from young mouse retinas can be transplanted, and can form photoreceptors in adult retinas. These cells can be grown in tissue culture, but can no longer form photoreceptors. We have used microarrays to investigate differences in gene expression between cultured retinal progenitor cells (RPCs) that have lost photoreceptor potential, postnatal day 1 (pn1) retinas and the postnatal day 5 (pn5) retinas that contain transplantable photoreceptors. We have also compared FACS sorted Rho-eGFP expressing rod photoreceptors from pn5 retinas with Rho-eGFP negative cells from the same retinas. We have identified over 300 genes upregulated in rod photoreceptor development in multiple comparisons, 37 of which have been previously identified as causative of retinal disease when mutated. It is anticipated that this research should bring us closer to growing photoreceptors in culture and therefore better treatments for RD. This dataset is also a resource for those seeking to identify novel retinopathy genes in RD patients. We extracted whole retinas from postnatal day 1 (Pn1) and postnatal day 5 (Pn5) mice, and compared them with cultured RPCs derived from pn5 retinas, using Affymetrix mouse 430A_2 arrays. We also extracted cells from Rho-eGFP Pn5 retinas and FACS sorted them. GFP+ve cells represent immature rod photoreceptors, as they express the Rho-eGFP fusion protein, which is only expressed in rods. GFP-ve cells represent all other retinal neurons. These samples were amplified and compared using Affymetrix mouse 430A_2arrays, by Source Biosciences GMBH, Berlin, Germany. Results from immature rods were then compared with those from other retinal neurons, while results from whole Pn5 retinas were compared with Pn1 retinas (which don't yet express rod specific genes), and RPCs, which are glial precursors. RPCs were also compared with Pn1 retinas. Genes which showed changed expression profiles in at least 3/4 of comparisons were prioritised for further investigation.
2015-01-20 | E-GEOD-59201 | biostudies-arrayexpress
Project description:Retinal degenerative diseases are some of the leading causes of blindness with few treatments. Various cell-based therapies have aimed to slow the progression of vision loss by preserving light-sensing photoreceptor cells. A subretinal injection of human neural progenitor cells (hNPCs) into the Royal College of Surgeons (RCS) rat model of retinal degeneration has aided in photoreceptor survival, though the mechanisms are mainly unknown. Identifying the retinal proteomic changes that occur following hNPC treatment will lead to better understanding of neuroprotection. To mimic the retinal environment following hNPC injection, a co-culture system of retinas and hNPCs was developed. Less cell death occurred in RCS retinal tissue co-cultured with hNPCs than in retinas cultured alone, suggesting that hNPCs provide retinal protection in vitro. Comparison of ex vivo and in vivo retinas identified NRF2-mediated oxidative response signaling as an hNPC-induced pathway. This is the first study to compare proteomic changes following treatment with hNPCs in both an ex vivo and in vivo environment, further allowing the use of ex vivo modeling for mechanisms of retinal preservation. Elucidation of the protein changes in the retina following hNPC treatment may lead to the discovery of mechanisms of photoreceptor survival and its therapeutic for clinical applications.
2018-12-17 | PXD011491 | Pride