Gene expression profile at single cell level of microglia sorted from rats brain with chronic cerebral hypoperfusion
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE234247 | GEO | 2024/08/26
REPOSITORIES: GEO
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Project description:Hippocampus miRNA profiles in chronic cerebral-hypoperfusion rats
| PRJNA595889 | ENA
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
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
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
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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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
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
Project description:This study aims at a comprehensive understanding of the genomic program activated during early-phase of collateral vessel growth in a rat model for cerebral adaptive arteriogenesis (3-VO). While arteriogenesis constitutes a promising therapeutic concept for cerebrovascular ischemia, genomic profiles essential for therapeutic target identification were analysed solely for collateral arteries of the heart and periphery. Despite challenging anatomical conditions of the brain the 3-VO model allows identification of differentially expressed genes during adaptive cerebral arteriogenesis by selective removal of the posterior cerebral artery (PCA). Experiment Overall Design: Using an established rat model of nonischemic cerebral hypoperfusion (3-VO) (Busch, Buschmann; 2003), RNA was extracted from isolated ipsilateral PCA. Pooled RNAs from groups of intact (0h), sham and 3-VO animals 24h and 3 days after surgery, were hybridised repeatedly for an extensive genome screen of 15866 genes applying standardized Affymetrix technology. For each Array total RNA from 8 animals was processed, pooled and hybridized to a Rat230A GeneChip per group. These groups were classified as follows: intact control (N=3), 24h3VO (N=3); 24h sham (N=3), 3days3VO (N=3); and 3days sham(N=3). Hybridization, washing, antibody amplification, staining, and scanning of probe arrays were performed according to the Affymetrix Technical Manual. Probe arrays were scanned using the GeneChip System (Hewlett-Packard, Santa Cruz, CA)(Affymetrix) and raw data were processed using GCOS and normalized to a global intensity of 500.
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Project description:Microglia modulate cerebral blood flow and cerebrovascular reactivity, but the mechanisms remain elusive. Here we show that pharmacological or genetic method induced microglia-ablation, which causes reduction of the microglia-expressed ATP/ADP-hydrolyzing ectonucleotidase CD39, elevates the cerebral blood flow baseline, while reducing the cerebral blood flow change to whisker stimulation and intra-cisterna magna injection of ATP, but not adenosine. Microglia P2ry12 inhibition with clopidogrel increased basal cerebral blood flow and the effect was abolished in microglia specific CD39 knockout mice. P2ry12 knockout mice show reduced cerebral blood flow changes to whisker stimulation or intra-cisterna magna injection of ATP. Microglia-specific deletion of CD39 or its pharmacological inhibition reproduces the effects of microglia ablation on cerebral blood flow and attenuates whisker stimulation-induced adenosine concentration increase in contralateral barrel cortex. These results suggest that microglia-dependent adenosine production is an integral component of the brain purinergic signaling system that governs neurovascular coupling.
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Project description:Cerebral malaria is a pathology involving inflammation in the brain. There are many immune cell types activated during this process, but there is little information on the contribution of microglia, the brain resident macrophages, to this severe complication. We have examined the responses of microglia in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA. Genome wide transcriptomic analysis of these cells revealed that thousands of transcripts were differentially expressed at two different time points during the infection. The analysis indicated that proliferation of microglia was a dominant feature before the onset of ECM, and supporting this, we observed an increase in numbers of these cells in the brain. When cerebral malaria symptoms were manifest, genes involved in immune responses and chemokine production were upregulated, which were possibly driven by Type I Interferon. Together, our data offer a unique insight into the responses of microglia in the brain during ECM.
2016-12-19 | GSE86082 | GEO