E-GEOD-50059
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA215899
PROVIDER: E-GEOD-50059 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-50059-analysis-methods.tsv | Tabular | |||
| E-GEOD-50059-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-50059-configuration.xml | Xml | |||
| E-GEOD-50059-percentile-ranks.tsv | Tabular | |||
| E-GEOD-50059.condensed-sdrf.tsv | Tabular |
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Similar Datasets
Project description:Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis
| PRJNA215899 | ENA
Project description:Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor. Z/Edn2 females were crossed to Six3-Cre; Six3-Cre males. Postnatal P8 pups were genotyped for the Z/Edn2 allele by detection of Laz-Z activity in tail clips. Retinas from 2 - 3 pups were pooled for each data point.
2014-01-01 | E-GEOD-50059 | biostudies-arrayexpress
Project description:Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor.
2014-01-01 | GSE50059 | GEO
Project description:Endothelial tip cells guiding tissue vascularization are primary targets for angiogenic therapies. Whether tip cells require differential signals to develop their complex branching patterns remained unknown. Here we show that diving tip cells invading the neuroretina (D-tip cells) are distinct from tip cells guiding the superficial retinal vascular plexus (S-tip cells). D-tip cells have a unique transcriptional signature, including high TGFβ signaling, and acquire blood-retina barrier properties. Endothelial deletion of TGFβ receptor I (Alk5) inhibits D-tip cell identity acquisition and deep vascular plexus formation. Loss of endothelial ALK5, but not of the canonical SMAD effectors, leads to aberrant contractile pericyte differentiation, and hemorrhagic vascular malformations. Our data reveal stage-specific tip cell heterogeneity as a requirement for retinal vascular development and suggest that noncanonical-TGFβ signaling could improve retinal revascularization and neural function in ischemic retinopathy.
2021-07-16 | GSE175895 | GEO
Project description:Objective: To determine the effects of age and topographic location on gene expression in human neural retina. Methods: Macular and peripheral neural retina RNA were isolated from human donor eyes for DNA microarray and quantitative RTPCR analyses. Results: Total RNA from human donor retina preserved integrity. Hierarchic clustering analysis demonstrates the gene expression profiles of young, old, macula and peripheral retina cluster into four distinct groups. Genes which are highly expressed in macular, peripheral, young or old retina are identified, including inhibitors of Wnt Signaling Pathway (DKK1, FZD10 and SFRP2) shown preferably expressed in the periphery. Conclusions: The transcriptome of the human retina is affected by age and topographic location. Wnt pathway inhibitors in the periphery may maintain peripheral retinal cells in an undifferentiated state. Understanding the effects of age and topographic location on gene expression may lead to the development of new therapeutic interventions for age-related eye diseases. Twleve youang and older retinal macular or prepheral RNA samples are used for DNA microarray study to compare the effects of aging and anatomic location on gene expression in human retina.
2015-05-27 | E-GEOD-32614 | biostudies-arrayexpress
Project description:Various retinal disorder such as glaucomatous, retinal ischemia reperfusion, and traumatic optic neuropathy, are involved in the pathogenesis of neurodegeneration via glutamate exicitotoxicity. However, the proteomic characteristics and modulation of the neural-microenvironment with NMDA-induced neurodegeneration in retina and optic nerve remain partly understood. We established a protein sketch of NMDA-induced injury by comparing the proteomes of the PBS-operated, NMDA-operated and control groups. We carried out mass spectrometry-based label-free quantitative proteomics to investigate the exicitotoxic neurodegeneration mechanisms and identify key proteins that regulated neural cell death related signaling pathway in retina and optic nerve spatially. Using LC-MS/MS proteomics analysis, in total, we identified 3532 proteins in retina, 2593 proteins in optic nerve. According to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), the protein changes and energy metabolism in retina and optic nerve tissue were comprehensively evaluated.
2021-12-30 | PXD022729 | Pride
Project description:Various retinal disorder such as glaucomatous, retinal ischemia reperfusion, and traumatic optic neuropathy, are involved in the pathogenesis of neurodegeneration via glutamate exicitotoxicity. However, the proteomic characteristics and modulation of the neural-microenvironment with NMDA-induced neurodegeneration in retina and optic nerve remain partly understood. We established a protein sketch of NMDA-induced injury by comparing the proteomes of the PBS-operated, NMDA-operated and control groups. We carried out mass spectrometry-based label-free quantitative proteomics to investigate the exicitotoxic neurodegeneration mechanisms and identify key proteins that regulated neural cell death related signaling pathway in retina and optic nerve spatially. Using LC-MS/MS proteomics analysis, in total, we identified 3532 proteins in retina, 2593 proteins in optic nerve. According to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), the protein changes and energy metabolism in retina and optic nerve tissue were comprehensively evaluated.
2021-12-30 | PXD022466 | Pride
Project description:Objective: To determine the effects of age and topographic location on gene expression in human neural retina. Methods: Macular and peripheral neural retina RNA were isolated from human donor eyes for DNA microarray and quantitative RTPCR analyses. Results: Total RNA from human donor retina preserved integrity. Hierarchic clustering analysis demonstrates the gene expression profiles of young, old, macula and peripheral retina cluster into four distinct groups. Genes which are highly expressed in macular, peripheral, young or old retina are identified, including inhibitors of Wnt Signaling Pathway (DKK1, FZD10 and SFRP2) shown preferably expressed in the periphery. Conclusions: The transcriptome of the human retina is affected by age and topographic location. Wnt pathway inhibitors in the periphery may maintain peripheral retinal cells in an undifferentiated state. Understanding the effects of age and topographic location on gene expression may lead to the development of new therapeutic interventions for age-related eye diseases.
2015-05-27 | GSE32614 | GEO
Project description:The histone methyltransferase complex PRC2 controls key steps in developmental transitions and cell fate choices. However, its roles in vertebrate eye development remain unknown. Here we report that in Xenopus PRC2 regulates the progression of retinal progenitors from proliferation to differentiation. We show that the PRC2 core components are enriched in retinal progenitors and downregulated with differentiation. Knockdown of the PRC2 core component Ezh2 leads to reduced retinal progenitor proliferation in part due to upregulation of the cdk inhibitor p15Ink4b. In addition, while PRC2 knockdown does not alter eye patterning, retinal progenitor gene expression or expression of the neural competence factor Sox2, it does cause suppression of proneural bHLH gene expression, indicating that PRC2 is critical for the initiation of neural differentiation in the retina. Consistent with this, knocking down or blocking PRC2 function constrains the generation of most retinal neural cell types and promotes a Mueller glial cell fate decision. We also show that Wnt/?-catenin signaling acting through the receptor Frizzled 5, but independent of Sox2, regulates expression of key PRC2 subunits in the developing retina. This is consistent with a role for this pathway in coordinating proliferation and the transition to neurogenesis in the Xenopus retina. Our data establishes PRC2 as a regulator of proliferation and differentiation during eye development. Xenopus embryos were injected at the 8-cell stage with 5ng Ezh2 ATG MO or 5ng control MO (scrambled sequence of Ezh2 ATG MO) together with 400 pg mRNA for GFP as a lineage tracer. At stage 27, GFP-positive eyes were isolated by microdissection. Pools of 20-25 eyes were used to prepare total RNA for each sample on the microarray. 4 control and 4 Ezh2 ATG MO samples were hybridized to Agilent 1-color microarrays.
2013-05-30 | E-GEOD-47456 | biostudies-arrayexpress
Project description:<p>We sought to characterize cellular heterogeneity in the human cerebral cortex at a molecular level during cortical neurogenesis. We captured single cells and generated sequencing libraries using the C1TM Single-Cell Auto Prep System (Fluidigm), the SMARTer Ultra Low RNA Kit (Clontech), and the Nextera XT DNA Sample Preparation Kit (Illumina). We performed unbiased clustering of the single cells and further examined transcriptional variation among cell groups interpreted as radial glia. Within this population, the major sources of variation related to cell cycle progression and the stem cell niche from which radial glia were captured. We found that outer subventricular zone radial glia (oRG cells) preferentially express genes related to extracellular matrix formation, migration, and stemness, including <i>TNC</i>, <i>PTPRZ1</i>, <i>FAM107A</i>, <i>HOPX</i>, and <i>LIFR</i> and related this transcriptional state to the position, morphology, and cell behaviors previously used to classify the cell type. Our results suggest that oRG cells maintain the subventricular niche through local production of growth factors, potentiation of growth factor signals by extracellular matrix proteins, and activation of self-renewal pathways, thereby contributing to the developmental and evolutionary expansion of the human neocortex.</p> <p>For <b>study version 2</b>, we have updated this data set to include additional primary cells that we infer to represent microglia, endothelial cells, and immature astrocytes, as well as additional cells from the developing neural retina, and from iPS-cell derived cerebral organoids. The genes distinguishing these cell populations may reveal biological processes supporting the diverse functions of these cell types as well as vulnerabilities of specific cell types in human genetic diseases and in viral infections.</p> <p>For <b>study version 3</b>, we have updated the data set to include additional primary cells, including those published in Nowakowski, et al., Science 2017: "Spatiotemporal Gene Expression Trajectories Reveal Developmental Hierarchies of the Human Cortex" (<i>in press</i>)</p>
| phs000989 | dbGaP