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

Htr2b Enhances the Phagocytosis of Brain Macrophages and Alleviates Brain Injury after Stroke

Project description:Brain myeloid cells, including infiltrating monocyte-derived macrophages (MDMs) and resident microglia play critical roles in regulating debris clearance following ischemic brain injury, shaping neuroinflammation evolution and neurological outcome, yet the underlying mechanism remains elusive. In this study, using single-cell RNA sequencing and fate mapping, we identified serotonin receptor Htr2b+ MDMs as a pivotal subgroup involved in resolving neuroinflammation within the ischemic penumbra. In addition, we find significant accumulation of Htr2b+ MDMs with enhanced phagocytosis and inflammation-resolving gene signatures in the peri-infarct region. Mechanistically, Htr2b activation promotes nuclear translocation of Tfe3, a key lysosomal regulator, enhancing lysosomal biogenesis and supporting sustained phagocytic activity. Myeloid-specific Htr2b ablation impairs debris clearance, exacerbates neuroinflammation and ischemic injury, while pharmacological Htr2b agonism or Tfe3 activation restores the lysosomal competence of brain MDMs and improves post-stroke neurological outcome. In conclusion, we demonstrate a novel Htr2b+ MDM subset that integrates serotonin signaling to license their intrinsic phagocytosis function, alleviating ischemic brain injury.

2026-07-04 | PXD074993 | Pride

Single-cell RNA-seq profiling of brain myeloid cells following ischemic stroke in Ms4a3-specific Htr2b conditional knockout mice

Project description:Brain myeloid cells, including infiltrating monocyte-derived macrophages (MDMs) and resident microglia, play essential roles in debris clearance and neuroinflammation resolution following ischemic brain injury. However, the molecular mechanisms governing the functional heterogeneity of these populations remain poorly understood. In this study, we performed single-cell RNA sequencing (scRNA-seq) to characterize the cellular and transcriptional landscape of immune and non-immune cells in the ischemic brain using a myeloid-specific Htr2b conditional knockout model. Htr2b^flox/flox mice and Htr2b^ERCre; Ms4a3-Cre mice were treated with tamoxifen to induce myeloid-lineage-specific recombination, followed by transient middle cerebral artery occlusion (tMCAO). Ipsilateral brain hemispheres were collected at 3 days post-stroke, a critical time point for inflammatory evolution and macrophage infiltration. Single-cell suspensions were generated from ischemic hemispheres, and both immune and non-immune cells were captured . This dataset enables detailed analysis of myeloid cell states, fate-mapped monocyte-derived macrophages, and the impact of Htr2b deletion on post-ischemic neuroinflammation, providing a valuable resource for studying immune regulation in ischemic stroke.

2026-07-03 | GSE318800 | GEO

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

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

| PRJNA1283135 | ENA

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

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

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