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Hippocampus-specific transcriptome profiling after severe cerebral hypoperfusion in mice

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

PROVIDER: PRJNA926913 | ENA |

REPOSITORIES: ENA

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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 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

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Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

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

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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

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Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats

Project description:Chronic cerebral hypoperfusion (CCH) is a well-known risk factor for vascular dementia and other neurodegenerative disease, for which there are currently no effective medications available. MicroRNA (miRNA) are noncoding RNAS mediating post-translational silencing of genes, and has been extensively studied for their involvement in neurodegenerative disease. However, little is known about their roles in vascular dementia (VaD). In this work, a bilateral common carotid arteries occlusion (2-VO) surgery in rats was employed to induced CCH related cognitive dysfunction. Four months later, the hippocampi were dissected from 2-VO and sham operated rats for high-throughput profiling of miRNAs. Twelve differentially expressed miRNAs were identified according to a cutoff of |log2(Fold Change)|≥1 and p＜0.05. GO analysis of target genes revealed that the most relevant biological processes included the regulatory region nucleic acid binding, histone acetyltransferase binding, organic acid transmembrane transporter activity, L-amino acid transmembrane transporter activity. The cellular structure mainly included histone deacetylation complexes, endosomes, Golgi membranes, etc. And the involved molecular processes mainly included axon development, organ morphogenesis, macromolecular modification, regulation of neuron projection development, neuron development. This study provides a framework for understanding the alternations in hippocampus miRNA profiles underwent hypoxia insult.

2019-12-17 | GSE142087 | GEO

Cortex-specific transcriptome profiling after deeper cerebral hypoperfusion in mice

Project description:Cortex-specific transcriptome profiling after deeper cerebral hypoperfusion in mice

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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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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.

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