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

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

PROVIDER: PRJNA1106380 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28847273_1.fastq.gz	Fastqsanger.gz
	SRR28847273_2.fastq.gz	Fastqsanger.gz
	SRR28847274_1.fastq.gz	Fastqsanger.gz
	SRR28847274_2.fastq.gz	Fastqsanger.gz
	SRR28847275_1.fastq.gz	Fastqsanger.gz

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

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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.

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