Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chronic Cerebral Hypoperfusion Induces Pathological Venous Remodeling via EPAS1 Regulation

ABSTRACT: Chronic Cerebral Hypoperfusion Induces Pathological Venous Remodeling via EPAS1 Regulation

PROVIDER: PRJNA1096111 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR28552118_1.fastq.gz	Fastqsanger.gz
	SRR28552118_2.fastq.gz	Fastqsanger.gz
	SRR28552119_1.fastq.gz	Fastqsanger.gz
	SRR28552119_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 51

Similar Datasets

Chronic Cerebral Hypoperfusion Induces Pathological Venous Remodeling via EPAS1 Regulation

Project description:Chronic cerebral hypoperfusion, induced by bilateral common carotid artery stenosis (BCAS), models the underlying cause of vascular dementia. We used single-cell transcriptomics to identify endothelial subtype-specific responses to BCAS in the mouse prefrontal cortex. The most dynamic molecular changes were observed in venous endothelial cells, with upregulated pathways linked to vascular remodeling and angiogenesis. Cerebral hypoperfusion upregulated expression of the endothelial PAS domain protein 1 (Epas1 ) gene in venous endothelial cells, while exposure of human venous endothelial cells to 1% oxygen in vitro caused sustained nuclear translocation of EPAS1. Pharmacological inhibition of EPAS1 reduced abnormal venous sprouting and concomitantly dampened microglia activation. Among human subjects with mild cerebrovascular disease, there was a negative correlation observed between their circulating damaged endothelial cells (CECs) and cerebral blood flow levels. In addition, elevated levels of venous-origin CECs were detected in subjects with white matter lesions and were notably linked to poorer overall cognitive function. We conclude that venous endothelial cells are potential therapeutic targets for vessel normalization to mitigate vascular cognitive impairment caused by chronic cerebral hypoperfusion.

2025-05-27 | GSE263191 | GEO

RNAseq of mouse corpus callosum from WT or TRPA1-KO animals under chronic cerebral hypoperfusion

Project description:Chronic cerebral hypoperfusion is manifested in various CNS diseases accompanied by cognitive impairment, such as dementia, however the precise mechanism of chronic cerebral hypoperfusion-induced cognitive impairment remains unknown. Recently, transient receptor potential ankyrin 1 (TRPA1), activated by oxidative stress, was reported to be involved in the cerebrovascular diseases, therefore we investigated the pathophysiological role of TRPA1 in chronic cerebral hypoperfusion using a mouse bilateral common carotid artery stenosis (BCAS) model. Early cognitive impairment and white matter injury was induced by BCAS in TRPA1-knockout (TRPA1-KO) but not wild-type (WT) mice. For further investigation into the involvement of TRPA1 in chronic cerebral hypoperfusion, we conducted RNA sequence (RNAseq) in the corpus callosum from sham- and BCAS-operated WT and TRPA1-KO mice.

2023-08-08 | GSE201513 | GEO

Cortex-specific transcriptome profiling after deeper cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to cerebral cortex damage and glial activation after severe cerebral hypoperfusion.Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms. To investigate cortex-specific transcriptome profiling after severe cerebral hypoperfusion in mice

2023-03-09 | GSE210666 | GEO

Hippocampus-specific transcriptome profiling after severe cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to hippocampus damage and glial activation after severe cerebral hypoperfusion.Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms. To investigate hippocampus-specific transcriptome profiling after severe cerebral hypoperfusion in mice

2023-07-26 | GSE223580 | GEO

Cortex-specific epigenetic profiling of chromatin accessibility after deeper cerebral hypoperfusion in mice

Project description:Efforts to understand genetic variability involved in cortex damage and glial activation support a role for upstream regulation by epigenetic mechanisms. To investigate cortex-specific epigenetic profiling after severe cerebral hypoperfusion in mice

2023-10-17 | GSE215893 | GEO

Hippocampus-specific epigenetic profiling of chromatin accessibility after deeper cerebral hypoperfusion in mice

Project description:Efforts to understand genetic variability involved in hippocampus damage and glial activation support a role for upstream regulation by epigenetic mechanisms. To investigate hippocampus-specific epigenetic profiling after severe cerebral hypoperfusion in mice

2025-04-23 | GSE246972 | GEO

Brain microvessel-specific transcriptome profiling after severe cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to brain microvessel damage and glial activation after severe cerebral hypoperfusion. Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms.

2024-12-06 | GSE266214 | GEO

Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

Project description:Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

| PRJNA595889 | ENA

Gene expression profile at single cell level of microglia sorted from rats brain with chronic cerebral hypoperfusion

Project description:Microglia are considered as a heterogenous population in the brain tissues. We used single-cell RNA sequencing (scRNA-seq) to analyze the diversity of microglia in the rats with chronic cerebral hypoperfusion.

2024-08-26 | GSE234247 | GEO

Cerebral hypoperfusion exacerbates traumatic brain injury in male mice

Project description:Traumatic brain injury (TBI) has been postulated to initiate a disease process that interacts with vascular dysfunction. However, the combined effects of preexisting cerebral hypoperfusion and TBI remain poorly explored. This study aimed to investigate the combined effects of bilateral carotid artery stenosis (BCAS) and mild-moderate TBI on cerebral blood flow (CBF), cognitive function, histology, and transcriptomics in Swiss-Webster mice. Male and female mice underwent BCAS using steel microcoils around the carotid arteries, followed by TBI 30 days post coil implantation. CBF, spatial learning and memory, axonal damage, and gene expression profiles were assessed. BCAS led to a ~10% reduction in CBF, while TBI caused a similar decrease. However, mice exposed to both BCAS and TBI exhibited more pronounced reductions in CBF, associated with marked spatial learning and memory deficits, particularly in males. Axonal damage in male mice was also exacerbated by the combination of BCAS and TBI. Notably, females demonstrated differential vascular and cognitive responses to BCAS and TBI, suggesting sex-specific protective mechanisms. Single nuclei RNA sequencing revealed unique, cell type-specific gene expression alterations due to BCAS, TBI, or the combination. Moreover, BCAS and TBI induced significant gene expression changes in various cell types, hinting at complex cellular interactions following vascular challenges and trauma. The cellular and molecular interplay between hypoperfusion and TBI points to intricate vascular-neuronal interactions and potential avenues for targeted interventions.

2024-08-14 | GSE241690 | 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