Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sustaining microglial reparative function enhances stroke recovery [Bulk RNA-seq]

ABSTRACT: To investigate time-dependent changes in gene expression in microglia after ischemic stroke, we performed RNA-seq of FACS-sorted microglia from mouse brains at multiple time points after middle cerebral artery occlusion (MCAO).

ORGANISM(S): Mus musculus

PROVIDER: GSE319237 | GEO | 2026/03/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Sustaining microglial reparative function enhances stroke recovery [ATAC-seq]

Project description:To investigate time-dependent changes in the epigenetic chromatin state in microglia after ischemic stroke, we performed assay for transposase-accessible chromatin with sequencing (ATAC-seq) of microglia from mouse brains at multiple time points after middle cerebral artery occlusion (MCAO).

2026-03-11 | GSE319235 | GEO

Sustaining microglial reparative function enhances stroke recovery [scRNA-seq]

Project description:To investigate microglial heterogeneity and the effects of Zfp384 perturbation on brain cell populations after ischemic stroke, we performed single-cell RNA-seq of microglia and total brain cells from mouse brains at multiple conditions after middle cerebral artery occlusion (MCAO).

2026-03-11 | GSE319238 | GEO

Sustaining microglial reparative function enhances stroke recovery [HiChIP]

Project description:To detect chromatin loops maintaining genomic interactions among enhancer and promoter regions in microglia after ischemic stroke, we performed H3K27ac HiChIP of FACS-sorted CD45intCD11bint microglia from sham-operated and post-ischemic day 6 mouse brains.

2026-03-11 | GSE319240 | GEO

Sustaining microglial reparative function enhances stroke recovery [CUT&Tag]

Project description:To investigate YY1 and ZFP384 binding in microglia and the microglial cell line after ischemic stroke, we performed cleavage under targets and tagmentation (CUT&Tag) analysis using anti-YY1 and anti-ZFP384 antibodies.

2026-03-11 | GSE319239 | GEO

TGFβ-activated kinase 1-dependent microglial and macrophage responses aggravate long-term outcomes after ischemic stroke

Project description:Microglia/macrophages (Mi/MΦ) can profoundly influence stroke outcomes by acquiring functionally dominant phenotypes (pro-inflammatory or anti-inflammatory; neurotoxic or neuroprotective). Identification of the molecular mechanisms that dictate the functional status of Mi/MΦ after brain ischemia/reperfusion may reveal novel therapeutic targets for stroke. We hypothesized that activation of TGFβ-activated kinase 1 (TAK1), a key MAP3K upstream of multiple inflammation-regulating pathways, drives Mi/MΦ towards a pro-inflammatory phenotype and potentiates ischemia/reperfusion brain injury. Young adult mice were subjected to 1 h of middle cerebral artery occlusion (MCAO) followed by reperfusion. TAK1 was targeted by tamoxifen-induced Mi/MΦ-specific knockout (mKO). Mi/MΦ functional status and brain inflammatory profiles were assessed 3 days after MCAO by RNA-seq of flow cytometry-sorted brain Mi/MΦ. The results showed that TAK1 promotes ischemia/reperfusion-induced inflammation, brain injury, and maladaptive behavior by enhancing pro-inflammatory and neurotoxic Mi/MΦ responses.

2020-03-10 | GSE141972 | GEO

Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery

Project description:<p>Ischemic stroke recovery involves dynamic interactions between the central nervous system and infiltrating immune cells. Peripheral immune cells compete with resident microglia for spatial niches in the brain, but how modulating this balance affects recovery remains unclear. Here, we use PLX5622 to create spatial niches for peripheral immune cells, altering the competition between infiltrating immune cells and resident microglia in male mice following transient middle cerebral artery occlusion (tMCAO). We find that early-phase microglia attenuation promotes long-term functional recovery. This intervention amplifies a subset of monocyte-derived macrophages (RAMf) with reparative properties, characterized by high expression of GPNMB and CD63, enhanced lipid metabolism and pro-angiogenic activity. Transplantation of RAMf into stroke-affected mice improves white matter integrity and vascular repair. We identify Mafb as the transcription factor regulating the reparative phenotype of RAMf. These findings highlight strategies to optimize immune cell dynamics for post-stroke rehabilitation.</p>

2025-02-20 | MTBLS12240 | MetaboLights

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Protects Against Ischemic Stroke by Inhibiting M1 Microglia Polarization through Let-7b-5p/HMGA2/NF-κB Signaling Pathway

Project description:Modulating M1/M2 polarization is a potential therapy for treating ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS) held the capacity to regulate astrocytic polarization, but little is known about rTMS effects on microglia. Therefore, the present study aimed to investigate whether and how rTMS influence microglia polarization in ischemic stroke models. The 10-Hz rTMS was applied to transient middle cerebral artery occlusion (MCAO) rats and oxygen and glucose deprivation/ reoxygenation injured BV2 cells. Western blot, immunofluorescence and ELISA were used to detect M1/M2 markers. High-throughput sequencing, RT-PCR and FISH staining were adopted to test microRNA changes. The 10-Hz rTMS inhibited ischemia/reperfusion induced M1 microglia and significantly increased let-7b-5p. HMGA2 was proved to be the target protein of let-7b-5p and its downstream NF-κB signaling pathway were inhibited by rTMS. Microglia culture medium (MCM) collected from rTMS treated microglia had low TNF-α but high IL-10 concentration, leading to reduced neural death, minor ischemic volumes and improved functional recovery of MCAO animals. However, knockdown of let-7b-5p by antagomir reversed rTMS effects on microglia. In conclusion, high-frequency rTMS could improve functional recovery through inhibiting M1 microglia polarization via regulating let-7b-5p/HMGA2/NF-κB signaling pathway in cerebral ischemic stroke models.

2022-08-10 | GSE192910 | GEO

Gene expression profiles of endothelium, microglia and oligodendrocytes in hippocampus of post-stroke depression rat at single cell resolution

Project description:Post-stroke depression (PSD) is a common but severe mental complication after stroke. However, the cellular and molecular understanding of PSD is still yet to be illustrated. In current study, we prepared PSD rat model (MD) via unilateral middle cerebral artery occlusion (MCAO) and chronic stress stimulation (DEPR), and isolated hippocampal tissues for single cell sequencing of 10x Genomics Chromium. This study characterized the single cell expression profile of hippocampal PSD, and unmask the differential expressed genes of endothelium, microglia and oligodendrocytes, emphasizing the crosstalk among them to provide theoretical basis for the in-depth mechanism research and drug therapy of PSD.

2023-05-24 | GSE232936 | GEO

TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2

Project description:Stroke is a kind of cerebrovascular disease with high mortality. TMAO has been shown to aggravate stroke outcomes, but its mechanism remains unclear. Mice were treated with TMAO in normal saline by oral gavage for 14 consecutive days. Then, mice were made into MCAO models. Neurological score, infarct volume, neuronal damage and markers associated with inflammation were assessed. Since microglia played a crucial role in stroke, microglia of MCAO mice were isolated for high-throughput sequencing to identify the most differentially expressed gene following TMAO treatment. Afterward, the downstream pathways of TMAO were investigated using primary microglia. Our results demonstrated that TMAO promoted the release of inflammatory cytokines in the brain of MCAO mice and promoted the activation of OGD/R microglial inflammasome, thereby exacerbating stroke outcomes. FTO/IGF2BP2 inhibited NLRP3 inflammasome activation in OGD/R microglia by downregulating the m6A level of NLRP3, TMAO can inhibit the expression of FTO and IGF2BP2, thus promoting the activation of NLRP3 inflammasome in OGD/R microglia. In conclusion, these results demonstrated that TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2.

2023-09-06 | GSE216349 | GEO

Retinoid X Receptor as a Mediator of Post Stroke Recovery by Reversing Age-Associated Phenotypes of Microglia/Hematogenous Macrophages

Project description:After stroke, microglia/blood-derived macrophages, together MF, clear dead cells and cellular debris in the infarcted brain through phagocytosis as an essential part of the repair/recovery process. However, the phagocytic capability of MF declines with age. Furthermore, aged MF become overactivated in response to stroke, enhancing secondary brain injury. Now, demonstrate that by reversing the age-related dysfunctions in MF through activating the retinoid x receptor (RXR), the recovery after stroke in the aged brain could be improved. Using RNA sequencing, we compared the transcriptomes between MF isolated from the brains of young and aged mice. We observed higher levels of pro-inflammatory genes and lower levels of phagocytosis-facilitating genes (Cd206, Cd36) expressed by aged MF. Meanwhile, the treatment with RXR agonist bexarotene (BEX) reversed the signature genes of microglia aging in the aged MF. With the in vivo phagocytosis model, we showed that BEX enhanced the phagocytic ability of aged MF. Using mouse MCAo stroke model, we established that BEX improved sensorimotor and cognitive recovery after MCAo in a myeloid-RXRa-specific and -dependent manner. In conclusion, we showed that activating RXRa partially restores age-related MF dysfunctions and that RXRa deficiency in MF limits the therapeutic effect of RXR in improving post-stroke recovery in the aged brain

2025-09-17 | GSE287142 | 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