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

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

PROVIDER: PRJNA1149769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30298118_1.fastq.gz	Fastqsanger.gz
	SRR30298118_2.fastq.gz	Fastqsanger.gz
	SRR30298119_1.fastq.gz	Fastqsanger.gz
	SRR30298119_2.fastq.gz	Fastqsanger.gz
	SRR30298120_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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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.

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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.

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