Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of Wild type and Plagl1 knock out retina at P7

ABSTRACT: Plagl1 controls Muller glial cells proliferation in the retina. We used single cell RNA sequencing (scRNA-seq) to analyze the prolirative state of Muller glial cells and identify the signals that might be involved in this process

ORGANISM(S): Mus musculus

PROVIDER: GSE228191 | GEO | 2024/03/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profile at single cell level of Wild type and Plagl1 knock out retina at P7

Project description:Gene expression profile at single cell level of Wild type and Plagl1 knock out retina at P7

| PRJNA948461 | ENA

Ciliary neurotrophic factor induces genes associated with inflammatory response and gliosis in the retina: A gene profiling study of flow-sorted, Muller (glial) cells

Project description:Our data suggest that CNTF remodels the transcription profile of Muller (glial) cells leading to induction of networks associated with transcription, cell cycle regulation and inflammatory response. CNTF also appears to function as an inducer of gliosis in the retina. These studies provide new insights into the biological functions of cytokines in the retina. Muller glial cells treated with CNTF for 1 and 3 days

2011-08-31 | E-GEOD-27195 | biostudies-arrayexpress

Characterization of the transcriptomic profile of Plagl1+/-pat retina

Project description:Retinal damage triggers reactive gliosis in Müller glia across vertebrate species, but only in regenerative animals, such as teleost fish, do Müller glia initiate repair; proliferating and undergoing neurogenesis to replace lost cells. We found that Plagl1, a maternally imprinted gene, is dynamically regulated in reactive Müller glia post-insult, with transcript levels transiently increasing before stably declining. To study Plagl1 retinal function, we examined Plagl1+/-pat null mutants postnatally, revealing defects in retinal architecture, visual signal processing and a reactive gliotic phenotype. Plagl1+/-pat Müller glia proliferate ectopically and give rise to inner retinal neurons and photoreceptors. Transcriptomic and ATAC-seq profiles revealed similarities between Plagl1+/-pat retinas and neurodegenerative and injury models, including an upregulation of pro-gliogenic and pro-proliferative pathways, such as Notch, not observed in wild-type retinas Plagl1 is thus an essential component of the transcriptional regulatory networks that retain mammalian Müller glia in quiescence.

2021-05-06 | GSE173942 | GEO

Characterization of the transcriptomic profile of Plagl1+/-pat retina

Project description:Characterization of the transcriptomic profile of Plagl1+/-pat retina

| PRJNA727582 | ENA

Characterization of the chromatin accessibility profile of Plagl1+/-pat retina

2021-05-05 | GSE173853 | GEO

Expression data from adult mouse normal and damaged retina from B6 and 129 mouse strains

Project description:Retinal damage causes proliferation of Muller glia, but the degree of proliferation depends on mouse strains. Muller glial proliferation was significantly promoted by the addition of GSK3 inhibitor in 129, but not in B6. We used retinal explant culture as a model for retinal damage which caused preferential photoreceptor death in a few days. We used microarrays to detail the global programme of gene expression regulating the proliferative potential of Muller glia after retinal damage. Total RNA from intact whole retina, retinal tissue cultured for three days, and retinal tissue cultured with chir99021 for three days was used. Retinal tissues from 10 weeks old mice were used.

2014-03-06 | E-GEOD-54056 | biostudies-arrayexpress

Characterization of the chromatin accessibility profile of Plagl1+/-pat retina

Project description:Characterization of the chromatin accessibility profile of Plagl1+/-pat retina

| PRJNA727312 | ENA

Hypoxia tolerance in the Norrin-deficient retina and the chronically hypoxic brain stuied at single-cell resolution

Project description:The mammalian central nervous system (CNS) is capable of tolerating chronic hypoxia, but cell type-specific responses to this stress have not been systematically characterized. In the Norrin-knockout (NdpKO) mouse, a model of familial exudative vitreoretinopathy (FEVR), developmental hypovascularization of the retina produces chronic hypoxia of inner nuclear layer (INL) neurons and Muller glia. We have used single-cell RNA sequencing, untargeted metabolomics, and metabolite labeling from 13C-glucose to compare wild type and NdpKO retinas. In NdpKO retinas, we observe gene expression responses consistent with hypoxia in Muller glia and retinal neurons, and we find a metabolic shift that combines reduced flux through the tricarboxylic acid cycle with increased synthesis of serine, glycine, and glutathione. We also used single-cell RNA sequencing to compare the responses of individual cell types in NdpKO retinas to those in the hypoxic cerebral cortex of mice that were housed for one week in a reduced oxygen environment (7.5% oxygen). In the hypoxic cerebral cortex, glial transcriptome responses most closely resemble the response of Muller glia in the NdpKO retina. In both retina and brain, vascular endothelial cells activate a previously dormant tip cell gene expression program, which likely underlies the adaptive neo-angiogenic response to chronic hypoxia. These analyses of retina and brain transcriptomes at single-cell resolution reveal both shared and cell-type-specific changes in gene expression in response to chronic hypoxia, implying both shared and distinct cell type-specific physiologic responses.

2019-04-19 | GSE125708 | GEO

Gene expression changes under cyclic mechanical stretch in rat retinal Muller cells

Project description:The retina is often subjected to tractional forces in a variety of conditions, for instance, pathological myopia, proliferative vitreoretinopathy. As the predominant glial element in the sensory retina, Muller cells are responsible for the homeostatic and metabolic support of retinal neurons and active players in virtually all forms of retinal injury and disease. Besides, Muller cells span the entire retinal thickness, extending from the inner to the outer limiting membranes, with cell bodies located in the inner nuclear layer and lateral processes expanding into the plexiform layers of the tissue. Because of this unique morphology, Muller cells can sense even minute changes in the retinal structure because of the mechanical stretching of their long processes or side branches. Thus, it’s reasonable to infer that Muller cells also participate in ocular diseases when the retina is overstretched. In this study, we aim to investigate the whole genome regulation of Muller cells under mechanical stretching, which may help in excluding possible molecular mechanisms that would account for many retinal diseases in which the retina is often subjected to mechanical forces. We used microarrays to identify patterns of gene expression changes induced by cyclic mechanical stretching in Muller cells.

2013-01-16 | GSE43516 | GEO

Ptbp1 deletion does not induce glia-to-neuron conversion in adult mouse retina and brain.

Project description:Purpose: scRNA-Seq was performed to profile changes in adult retina Muller glia cells and brain astrocytes after Ptbp1 deletion

2021-12-07 | GSE184933 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data