Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Consequences of reactive astrogliosis in vivo I

ABSTRACT: To investigate how molecularly induced reactive astrogliosis (MiRA) affects the transcriptomic signatures of astrocytes in the striatum, we used locally injected AAV2/5 GfaABC1D-RiboTag to purify and sequence astrocyte actively translated mRNAs in the striatum of the control and MiRA animals. Three weeks after AAV injection, striata were homogenized, and RNA was purified from (i) cleared lysate as the input and control, and (ii) astrocyte-specific ribosome-associated RNA precipitated via a hemagglutinin (HA) tag. Our analyses revealed that MiRA induces inflammatory signatures while downregulating the homeostatic genes in the striatal astrocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE305388 | GEO | 2026/09/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Consequences of reactive astrogliosis in vivo III

Project description:To investigate the role of LZK kinase activity in the astrocyte transcriptome, we locally injected AAV2/5 GfaABC1D-Myc-LZK, the kinase-dead mutant AAV2/5 GfaABC1D-Myc-LZK (K195A), or the viral baseline control AAV2/5 GfaABC1D-tdTomato into the dorsal striatum of C57BL/6NTac mice. AAV2/5 GfaABC1D-RiboTag was co-injected to enable purification and sequencing of actively translated astrocyte mRNAs. Three weeks after AAV injection, striata were homogenized, and RNA was purified from either cleared lysates, representing the input fraction, or HA-immunoprecipitated astrocyte-specific ribosome-associated RNA, representing the IP fraction. These analyses revealed that LZK kinase activity is required to induce transcriptomic changes associated with cell migration, apoptosis, proliferation, and synaptic transmission.

2026-09-23 | GSE336013 | GEO

Consequences of reactive astrogliosis in vivo IV

Project description:To investigate how molecularly induced reactive astrogliosis (MIRA) alters the transcriptome of the surrounding cells in the striatum, we locally injected AAV2/5 GfaABC1D-Cre-4X6T (MIRA) or AAV2/5 GfaABC1D-tdTomato (control) into the mouse striatum. Three weeks after AAV injection, fresh-frozen mouse striatal tissue was processed using the Chromium Nuclei Isolation Kit (10x Genomics, PN-1000494) according to the manufacturer's instructions. Isolated nuclei were immediately subjected to single-nucleus RNA sequencing (snRNA-seq) library preparation using the Chromium GEM-X Single Cell 3′ Reagent Kit (10x Genomics, PN-1000686). Approximately 20,000 nuclei were loaded per sample, targeting recovery of ~15,000 nuclei. Libraries from eight samples were pooled and sequenced on an Illumina NovaSeq X Plus platform using half of a 25B flow-cell lane. Our analyses revealed that MIRA induces transcriptomic changes primarily in glial cells, with comparatively smaller effects in neurons, and is associated with increased immune-related gene expression in microglia.

2026-09-23 | GSE336814 | GEO

Consequences of reactive astrogliosis in vivo II

Project description:To investigate how molecularly induced reactive astrogliosis (MiRA) affects regional differences among astrocytes, we used a combination of AAV PHP.eB CAG-flex-Rpl22 and AAV PHP.eB GfaABC1D-Cre-4X6T. We then performed RNA sequencing to examine the transcriptomic profiles of astrocytes isolated from the striatum, hippocampus, and prefrontal cortex in both control and MiRA mice at 4 weeks and 10 weeks post AAV injection. Our analyses revealed that while MiRA triggers a core set of differentially expressed genes, the inherent regional heterogeneity among astrocytes is largely preserved.

2026-09-23 | GSE305391 | GEO

Astrocyte-selective transduction with AAV5 viral vector does not exacerbate astrogliosis or alter tissue immune responses following spinal injury

Project description:Following contusive spinal injury astrocytes undergo inflammatory activation and proliferation in a process known as astrogliosis. Reactive astrocytes are attractive therapeutic targets as they sit central to many of the immune recruitment, injury response, and tissue healing processes of the spinal cord. However, methods of targeted expression of exogenous therapeutic genes within astrocytes must be validated to not alter the normal immunological involvement of astrocytes. To investigate the effect of transgene expression within astrocytes upon the immunological state of the contused cord, we injected the astrocyte-selective AAV5-GfaABC1D-dYFP reporter vector into an animal model of moderate contusive spinal cord injury. Bulk RNA microarrays were used to assess transcriptomic changes of the perilesional tissue.

2021-08-26 | GSE182796 | GEO

Astrocyte molecular signatures during Huntington’s disease progression and following huntingtin lowering with zinc finger protein transcriptional repressors

Project description:The Khakh laboratory used gfaABC1D-RiboTag AAVs to purify and sequence astrocyte actively translated mRNAs from Huntington's disease mouse models at several stages of the disease. Two weeks after AAV injection, striata were homogenized and RNA was purified from (i) cleared lysate as the input and control, and (ii) astrocyte-specific ribosome-associated RNA precipitated via a hemagglutinin (HA) tag. R6/2 mice are a fast developing model of Huntington's disease. Striatal cells show mutant HTT inclusions as early as 4 weeks of age. These mice show the first motor and cognitive symptoms around that age, but they become more evident around 8 week old and progressively impair until the mouse death that occurs around 13 weeks of age. Motor symptoms include increased paw clasping and grooming, impaired grip strength and rotarod performance, gait alterations, involuntary movements, etc. Cognitive impairment includes defects in learning and memory. NCAR mice are the healthy "non-carrier" controls for R6/2. They don't have unexpected phenotypes.

2020-01-08 | GSE124846 | GEO

Transcriptional analysis of murine cortical astrocytes with adeno-associated viral transduction with and without 4x6T miR cassette, vs transgenically labeled astrocytes

Project description:We generated adeno-associated Cre viral vectors with improved astrocyte-specific expression by including a cassette of miRNA targeting sequences (4x6T) to decrease off-target expression. We delivered these viruses in Ribotag mice using the PHP.eB serotype, either intracortically or systemically. We compared these samples with mice that received intracortical AAV2/5::GfaABC1D-Cre and transgenic Aldh1l1-CreERT2/Ribotag mice. We sequenced whole-tissue RNA as well as ribosomally-loaded astrocyte-enriched mRNA to assess cell-type specificity of viruses as well as virus-related transcriptomic changes.

2023-03-03 | GSE226366 | GEO

In vivo analysis of gene expression changes in mouse astrocytes after biomaterial injection into striatum

Project description:We conducted genome-wide RNA sequencing of immunoprecipitated specific ribosome-associated mRNA using RiboTag methods from mouse striatum following injection of a methyl cellulose biomaterial at 7, 14, 28, and 70 days after injection using AAV5 GfaABC1D-Rpl22HA to label astrocytes with RiboTag. Flow through samples were also processed to enable astrocyte gene enrichment analysis. Comparisons were also made between unloaded MC biomaterials and MC biomaterials delivering beta-hydroxybutyrate (BHB) at 7 and 28 days after injection. We also profiled transcriptomic responses of cultured mouse astrcoytes derived from differentiated mouse neural progenitor cells when fueled with BHB or glucose.

2026-08-26 | GSE344979 | GEO

In vivo analysis of astrocyte ribosome-associated mRNA after traumatic spinal cord injury

Project description:Analysis of gene expression by astrocytes or non-astrocyte cells in spinal cord injury (SCI) lesions may lead to the identification of molecules that impact on axon regrowth. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) from WT or STAT3-CKO astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples 14 days following SCI. DOI: 10.1038/nature17623 Young adult female mGFAP-Cre-RiboTag or mGFAP-Cre-RiboTag-STAT3-LoxP mice underwent severe crush SCI at thoracic level 10. 14 days following SCI, the central 3mm of the SCI lesion was extracted, homogenized and (i) astrocyte-specific ribosome-associated RNA (ramRNA) precipitated via a hemagglutinin (HA) tag targeted to either WT (n=4) or STAT3-CKO (n=3) astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples. Sex and age-matched mGFAP-Cre-RiboTag mice served as uninjured controls (n=4).

2016-03-30 | E-GEOD-76097 | biostudies-arrayexpress

Astrogliosis and miscommunication in ALS

Project description:Chronic activation of glial cells leads to the dysfunction and degeneration of motor and cortical neurons in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) with an unknown mechanism. To shed light on the molecular pathogenetic processes underlying the exordium and contribution of gliosis to disease onset and progression, we used cells, mice, and patient-derived cells modeling TDP-43, SOD1, and C9orf72-linked and sporadic ALS. We identify an initial phase of the disease marked by increased astrocyte proliferation, followed by a typical activation stage with elevated expression of pro-inflammatory genes. Using mouse genetics, we show that expression of mutant TDP-43 in astrocytes is necessary to cause gliosis and behavioral abnormalities. Mechanistically, we show that c-Myc gain-of-function drives astrocyte proliferation by promoting the release of EVs that nonetheless fail to provide trophic support to surrounding neurons. Our research reveals a novel functional role for c-Myc in astrocytes in the miscommunication from glia to neurons in ALS.

2026-06-29 | PXD064120 | Pride

Activation of a neural stem cell transcriptional program in parenchymal astrocytes

Project description:Neural stem cells, located in discrete niches in the adult brain, generate new neurons throughout life. These stem cells are specialized astrocytes, but astrocytes in other brain regions (parenchymal astrocytes) do not generate neurons under physiological conditions. After stroke, however, astrocytes in the mouse striatum undergo neurogenesis, triggered by decreased Notch signaling. Notch signaling can be experimentally depleted in mice by deleting the Notch-mediating transcription factor Rbpj. This dataset consists of single-cell RNA sequencing data of astrocytes isolated from the striatum (where astrocytes undergo neurogenesis in response to Rbpj deletion) or somatosensory cortex (where astrocytes don't complete neurogenesis in response to Rbpj deletion) of 4 mice. Cells were isolated from Cx30-CreER; R26-tdTomato; Rbpj(fl/fl) mice at three time points after tamoxifen-induced Rbpj deletion (2, 4, 8 weeks), and from Cx30-CreER; R26-tdTomato mice with intact Rbpj 3 days after tamoxifen. These time points span the transition from astrocyte through transit-amplifying cells to neuroblasts. The dataset contains 1) astrocytes from the striatum that initiate a neurogenic transcriptional program in response to Rbpj deletion and generate transit-amplifying cells and neuroblasts, and 2) astrocytes from the somatosensory cortex that initiate a neurogenic program in response to Rbpj deletion but fail to generate transit-amplifying cells or neuroblasts.

2020-08-01 | E-MTAB-9268 | biostudies-arrayexpress

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