Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HTR2B Enhances the Phagocytosis of Brain Macrophages and Alleviates Brain Injury after Stroke

ABSTRACT: This study employs single-cell RNA sequencing to investigate the dynamic changes in monocytic-macrophage populations in the brain following ischemic stroke. We analyzed brain tissues from mice subjected to middle cerebral artery occlusion (MCAO) for 3 days. Additionally, we compared the macrophage transcriptomes between Htr2bfl/fl and Lyz2creHtr2b mice to elucidate the impact of HTR2B deficiency on macrophage responses 3d-post-stroke. Our findings provide novel insights into the role of HTR2B in regulating macrophage behavior and its potential implications in stroke pathogenesis and recovery.

ORGANISM(S): Mus musculus

PROVIDER: GSE301044 | GEO | 2026/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single-cell transcriptomic analysis of microglia and brain cells after ischemic stroke

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

Expression data from rat (Sprague Dawley) brain subjected to MCAo.

Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study. Total RNA isolated from sham, MCAo and MCAo+nPLA rat brains, was pooled to minimize inter-individual variation and hybridized to each array of the RAE-230A or U34A GeneChipTM according to protocols described in the GeneChipTM expression analysis package (Affymetrix, CA).

2009-09-04 | E-GEOD-17929 | biostudies-arrayexpress

Expression data from rat (Sprague Dawley) brain subjected to MCAo.

2009-09-04 | GSE17929 | GEO

Tau exacerbates excitotoxic brain damage in an animal model of stroke

Project description:Neuronal excitotoxicity induced by aberrant excitation of glutamatergic receptors contributes to brain damage in stroke. Here, we show that tau-deficient (tau-/-) mice are profoundly protected from excitotoxic brain damage and neurological deficits following experimental stroke, using a middle cerebral artery occlusion (MCAO) with reperfusion model. Mechanistically, we show that this protection is due to site-specific inhibition of glutamate-induced and Ras/ERK-mediated toxicity by accumulation of Ras-inhibiting SynGAP1, which resides in a post-synaptic complex with tau. Accordingly, reducing SynGAP1 levels in tau-/- mice abolished the protection from pharmacologically induced excitotoxicity and MCAO-induced brain damage. Conversely, over-expression of SynGAP1 prevented excitotoxic ERK activation in wild-type neurons. Our findings suggest that tau mediates excitotoxic Ras/ERK signaling by controlling post-synaptic compartmentalization of SynGAP1.

2017-09-01 | GSE45703 | GEO

Effects of ketogenic diet and caloric restriction on ischemic tolerance

Project description:The ketogenic diet (KD) is used to treat a number of brain pathologies. In this study, we undertook detailed transcriptomic profiling of rat brain after KD and ischemic stroke to uncover effects of KD and its specific mechanisms. We evaluated how a 2-month KD affected gene expression in intact brain tissue and after middle cerebral artery occlusion (MCAO). We found transcriptional reprogramming in the brain after stroke and KD treatment. KD altered the expression of genes involved in the regulation of glucose and fatty acid metabolism, mitochondrial function, immune response, Wnt-associated signaling, stem cell development, and neurotransmission in both intact rats and after MCAO.

2024-10-11 | GSE272485 | GEO

Single cell RNA sequencing of mouse brain hematopoietic cells after brain ischemia model

Project description:We performed scRNA-seq of brain CD45+ hematopoietic cells from the brain of Cd300a-fl/fl and Cd300a-fl/fl Lys2-Cre mice 0, 1 and 3 hrs after the reperfusion of middle cerebral artery occlusion (MCAO).

2021-12-22 | GSE154396 | GEO

Obacunone alleviates ischemia-induced blood-brain barrier disruption and brain injury via targeting MIF signaling

Project description:Blood-brain barrier (BBB) breakdown is one of the hallmarks of stroke pathology, which is characterized by the death of brain capillary endothelial cells and the disassembly of intercellular tight junction. Damaged BBB is associated with poor stroke prognosis, and few treatment of BBB breakdown is applicable. Obacunone (Oba) is a highly oxygenated triterpenoid with known pharmacological activities on mitigating colonic epithelial cell injury, however whether Oba could be effective to endothelial cell integrity remains unknown. In the present study, with the use of transient middle cerebral artery occlusion (tMCAO) mice model, we found that gavage Oba significantly alleviated tMCAO-induced BBB leakage, brain injury and neurological deficit. In the oxygen-glucose deprivation (OGD) model of mice brain microvascular endothelial cells (MBMECs), synergistic application of Oba and ISO-1 revealed the protective effect of Oba against MBMECs monolayer leakage via inhibiting MBMECs-derived macrophage migration inhibitory factor (MIF). In mechanism, with the use of bulk RNA sequencing and a battery of molecular approaches, we found that inhibition of MIF by Oba attenuated the activation of pro-apoptotic signals, including P38 and RIPK1, and promoted the distribution of tight junction ZO-1 onto MBMECs membrane, which was accompanied with the upregulation of intracellular LCN2. In consistent, pharmacological inhibition of LCN2 by ZINC00640089 protected against OGD-induced MBMECs death and monolayer leakage. These results collectively conclude that Oba alleviates ischemia-induced BBB breakdown and brain injury via, at least partially, inhibiting MIF-mediated endothelial cell death and intercellular junction loss. Oba may represent a therapeutic candidate for neurological disorders caused by cerebral stroke.

2026-05-08 | GSE317846 | GEO

Single cell expression profiling of murine subventricular zone in adult brain three days after focal celebral ischemia

Project description:Ischemic stroke is a serious medical condition that leads to the onset of neurological symptoms such as loss of motor and cognitive functions. Focal cerebral ischemia (FCI) occurs due to the interrupted blood supply to the site of injury, resulting in the demise of brain cells. The subventricular zone (SVZ) is a source of stem and progenitor cells (NS/PCs), which proliferate and differentiate in multiple cell types in order to substitute the injured tissue. We isolated cells from the SVZ and the adjacent striatum three days after middle cerebral artery occlusion (MCAO) in order to map cellular changes and NS/PCs plasticity in adult brain upon injury. Expression profiling of the isolated tissue at the single cell level enables the identification of cell population subtypes in the region and their characteristic gene expression.

2021-01-01 | E-MTAB-9935 | biostudies-arrayexpress

Effect of transient focal ischemia on circular RNAs

Project description:To investigate the potential involvement of circRNA in ischemic pathophysiology, we performed a circRNA microarray in an established transient middle cerebral artery occlusion (MCAO) mouse model of stroke. We evaluated the expression of 1797 circRNAs in adult mice brain after tMCAO. In our study, 5 of the 1178 circRNAs analyzed in the circRNA array were up-regulated significantly, ≥1.5-fold, in ischemic cortex at 12 hours of reperfusion after MCAO compared with their levels in sham group.

2020-09-25 | GSE115697 | GEO

Mouse ischemic tolerance genomic analysis of the brain and blood.

Project description:Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia. The experiment is a comparison of multiple treatment groups with sampling at multiple time points. The objective is to identify differentially regulated genes associated with preconditioning. Time points are examined both following preconditioning alone and following subsequent ischemic challenge (middle cerebral artery occlusion (MCAO)). Brain ipsilateral cortex tissue and blood were collected and processed from each animal. 6 experimental conditions: (n=3-4 mice/condition) LPS treated (i.p. 0.2mg/kg) + ischemic challenge (45min MCAO) CpG treated (i.p. 0.8mg/kg) + ischemic challenge (45min MCAO) Saline treated (i.p.) + ischemic challenge (45min MCAO) brief ischemia (12 min MCAO) + ischemic challenge (45min MCAO) Sham of brief ischemia (12 min) + ischemic challenge (45min MCAO) Non-treated + ischemic challenge (45min MCAO) Time points: Pre-ischemic challenge 3hr 24hr 72hr Post-ischemic challenge 3hr 24hr Unhandled (6 mice)-BASELINE

2011-10-04 | E-GEOD-32529 | 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