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Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (RNA-Seq)

ABSTRACT: Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (RNA-Seq)

PROVIDER: PRJNA1149767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30298184_1.fastq.gz	Fastqsanger.gz
	SRR30298184_2.fastq.gz	Fastqsanger.gz
	SRR30298185_1.fastq.gz	Fastqsanger.gz
	SRR30298185_2.fastq.gz	Fastqsanger.gz
	SRR30298186_1.fastq.gz	Fastqsanger.gz

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Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (RNA-Seq)

Project description:Vascular cognitive impairment (VCI) is a major cause of dementia, characterized by cognitive dysfunction resulting from cerebrovascular disease. Chronic cerebral hypoperfusion (CCH) is a significant contributor to VCI, impacting regions such as the white matter and the hippocampus. Despite the known effects on these areas, the response of the striatum to CCH has been less explored. This study aims to elucidate the molecular and cellular mechanisms underlying striatal dysfunction following CCH. Using a mouse model of bilateral common carotid artery stenosis (BCAS), we observed microglial activation in the striatum, suggesting an inflammatory response. We employed RNA-seq and ATAC-seq to integrate transcriptomic and epigenomic data, identifying changes in gene expression and chromatin accessibility associated with CCH. Our analysis revealed upregulation of immune-related pathways and downregulation of neuronal activity pathways, highlighting distinct regulatory mechanisms in response to hypoperfusion. The results provide insights into the pathogenesis of ischemic brain injury and suggest potential therapeutic targets for VCI.

2025-01-08 | GSE275195 | GEO

Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (ATAC-Seq)

2025-01-08 | GSE275194 | GEO

Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (ATAC-Seq)

Project description:Integrated Analysis of Chromatin and Transcriptomic Profiling of Striatum After Cerebral Hypoperfusion in Mice (ATAC-Seq)

| PRJNA1149769 | ENA

Integrated analysis of chromatin and transcriptomic profiling of the striatum after cerebral hypoperfusion in mice.

Project description:BackgroundVascular cognitive impairment (VCI) is a significant contributor to dementia, yet the precise mechanisms underlying the cognitive decline associated with chronic cerebral hypoperfusion (CCH) remain unclear. This study investigated the molecular and epigenetic changes in the striatum, a brain region critical for motor function and cognition, following chronic hypoperfusion using a bilateral common carotid artery stenosis (BCAS) model in mice.MethodsRNA-seq was utilized to identify differentially expressed genes (DEGs) associated with hypoperfusion. In parallel, ATAC-seq was used to assess changes in chromatin accessibility within the striatum, providing insight into the epigenome and potential regulatory mechanisms. The integration of these datasets allowed us to correlate chromatin accessibility with transcriptional activity and to identify key transcription factors driving the observed gene expression changes.ResultsAnalysis of striatum-specific transcriptome revealed significant upregulation of immune response genes, particularly type II interferon signaling, and downregulation of neural activation pathways. Analysis of striatum-specific epigenome showed increased chromatin accessibility at promoters of immune-related genes. Integrated analysis highlighted PU.1 as a key transcription factor in upregulated pathways, while neural pathways lacked epigenetic regulation, revealing distinct molecular responses in the striatum following chronic hypoperfusion.ConclusionsOur findings indicate that upregulated pathways in the striatum following BCAS-induced CCH are driven by epigenetic changes, while downregulated pathways occur independently of these modifications. Additionally, PU.1 plays a critical role in mediating immune responses, offering a potential target for therapeutic intervention.

| S-EPMC11762485 | biostudies-literature

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

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

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

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

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

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