Single cell RNA sequencing data of brain myeloid cells after experimental stroke
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ABSTRACT:
PROVIDER: PRJNA1003446 | ENA |
REPOSITORIES: ENA
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Project description:Acute stroke triggers extensive changes to myeloid immune cell populations in the brain that may be targets for limiting brain damage and enhancing repair. Immunomodulatory approaches will be most effective with precise manipulation of discrete myeloid cell phenotypes in time and space. Here, we investigate how stroke alters mononuclear myeloid cell composition and phenotypes at single-cell resolution and key spatial patterns. Our results show that multiple reactive microglial states and monocyte-derived populations contribute to an extensive myeloid cell repertoire in post-stroke brains. We identify important overlaps and distinctions among different cell types/states that involve ontogeny- and spatial-related properties. Notably, brain connectivity with infarcted tissue underpins the pattern of local and remote altered cell accumulation and reactivity. Our discoveries suggest a global but anatomically governed brain myeloid cell response to stroke that comprises diverse phenotypes arising through intrinsic cell ontogeny factors interacting with exposure to spatially organized brain damage and neuro-axonal cues.
2024-05-22 | GSE240368 | GEO
Project description:Inflammation triggers secondary brain damage after stroke. The meninges and other CNS border compartments serve as invasion sites for leukocyte influx into the brain thus promoting tissue damage after stroke. However, the post-ischemic immune response of border compartments compared to brain parenchyma remains poorly characterized . Here, we deeply characterize tissue-resident leukocytes in meninges and brain parenchyma by flow cytometry, histology, and single cell transcriptomics after experimental stroke and discover that leukocytes respond differently to stroke depending on their site of residence. We thereby discover a unique phenotype of myeloid cells exclusive to the brain after stroke. These stroke-associated myeloid cells partially resemble neurodegenerative disease-associated microglia. They are mainly of resident microglial origin, partially conserved in humans and exhibit a lipid-phagocytosing phenotype. Blocking markers specific for these cells partially ameliorates stroke outcome thus providing a potential therapeutic target. The injury-response of myeloid cells in the CNS is thus compartmentalized, adjusted to the type of injury and may represent a therapeutic target.
2021-11-26 | GSE189432 | GEO
Project description:Infection is a major complication and cause of mortality and morbidity after acute stroke however the mechanisms are poorly understood. After experimental stroke the microarchitecture and cellular composition of the spleen are extensively disrupted resulting in deficits to immune function. We used microarray to determine differentially expressed genes in the spleens of mice after experimental stroke to determine contributers to immunosuppression after stroke.
2016-07-19 | GSE70841 | GEO
Project description:Infection is a major complication and cause of mortality and morbidity after acute stroke however the mechanisms are poorly understood. After experimental stroke the microarchitecture and cellular composition of the spleen are extensively disrupted resulting in deficits to immune function. We used microarray to determine differentially expressed genes in the spleens of mice after experimental stroke to determine contributers to immunosuppression after stroke. We extracted RNA from spleens from 3 mice 5 d after experimental stroke when we have shown peak disruption to cellular composition and also from spleens from 2 sham-operated control mice for comparison.
2016-07-19 | E-GEOD-70841 | biostudies-arrayexpress
Project description:This study determined the influence of myeloid cell Trim59 deficiency on experimental stroke outcomes and the cerebral proteomic profile using myeloid cell Trim59 conditional knockout (Trim59-cKO) mice, the middle cerebral artery occlusion/reperfusion ischemic model, and a label-free quantitative proteomic profiling technique.
2024-08-02 | PXD049258 | Pride
Project description:Infection is a major complication and cause of mortality and morbidity after acute stroke however the mechanisms are poorly understood. After experimental stroke the microarchitecture and cellular composition of the spleen are extensively disrupted resulting in deficits to immune function. We used microarray to determine differentially expressed genes in the spleens of mice after experimental stroke to determine contributers to immunosuppression after stroke.
2018-06-06 | GSE108875 | GEO
Project description:The secondary immune response to ischemic stroke progresses for days to weeks and involves glial and brain endothelium activation, recruitment of peripheral immune cells, and release of cytokines and chemokines. Whereas there is evidence that the acute inflammatory response contributes to the progression of ischemic brain injury, on the other hand, recent research points at a more multifaceted role of immune cells in brain ischemia, where immune cells participate in repair processes during the sub-acute and chronic stages. Here we used single-cell sequencing to gain deeper insights into the impact of ischemic stroke on signature and the heterogeneity of brain immune cells, endothelial cells and circulating leukocytes in mice.
2023-06-14 | GSE225948 | GEO
Project description:Stroke is still a major cause of death and disability worldwide. A better comprehension of stroke pathophysiology is fundamental to reduce its dramatic outcome. Our aim was to identify and verify gene expression changes that occur in the human brain after ischemia.
2021-12-31 | GSE162955 | GEO
Project description:We have used microarrays to investigate the changes in gene expression at various times after stroke. Our findings reported that gene expression screening can detect known and unknown transcriptional features of stroke. Brain samples were obtained from 9 patients who died from stroke, with the approval of the local Ethics Committee. The patients were aged between 51 and 86 years and had survived between 2-37 days following stroke. Tissue samples were taken from infarct and peri-infarcted zones while controls were obtained from the contralateral hemisphere. We established mRNA expression profiles of the damaged brain tissues between 2 to 6 days, 9 to 20 days, and 26 to 37 days after stroke. RNA from three stroke patients was pooled for each patient survival group.
2010-06-25 | E-GEOD-9391 | biostudies-arrayexpress
Project description:Expression data from stroke patients brain samples
| PRJNA683904 | ENA