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Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [microglia]

ABSTRACT: Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [microglia]

PROVIDER: PRJNA718328 | ENA |

REPOSITORIES: ENA

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Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin

Project description:Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin

| PRJNA718584 | ENA

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [Treg]

Project description:Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [Treg]

| PRJNA718317 | ENA

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [scRNA-seq]

Project description:Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [scRNA-seq]

| PRJNA718585 | ENA

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [microglia]

Project description:We cocultured Tregs in transwells with brain slices collected 5d after tMCAO in the lower compartment for 24h to activate Tregs. Tregs in the transwells were transferred to new wells with primary cultured microglia, and cocultured for 2d. Microglia were then collected for bulk RNAseq analyses. The results revealed roles of activated Tregs in polarizing microglia toward an anti-inflammatory and reparative phenotype.

2021-05-19 | GSE171102 | GEO

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [Treg]

Project description:The precise mechanisms underlying the salutary effects of regulatory T cells (Tregs) on long-term tissue repair after stroke remain elusive. Here, , we performed RNAseq analysis on sorted CD4+CD25+Foxp3(GFP)+ Tregs from the ischemic brain and blood of DTR stroke mice 14d after surgery and from the blood of sham DTR mice. The unique patterns of gene expression of brain-infiltrating Tregs exhibited a significant enrichment for genes with functions in immunoregulation and cell-cell interactions, especially the activation of phagocytes.

2021-05-19 | GSE171097 | GEO

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-19 | GSE171171 | GEO

Proteomic alterations in microglia with ischemic stroke and effect of LPS treatment

Project description:Ischemic stroke is a common acute CNS disorder leading to nearly half a million deaths per year in Europe. The high mortality is primarily owed to the limited treatment options of restoring blood flow in a narrow time window of several hours. Furthermore, inflammatory processes in the days and weeks after ischemic stroke contribute to tissue loss and neurological deficits. The key cells that influence and control this inflammatory cascade are microglia, the innate immune cells of the CNS. Microglia can be influenced and activated by e.g. lipopolysaccharide (LPS),a bacterial cell membrane component. It has been previously shown, that repetitive LPS stimuli prior to infarction (termed immunological preconditioning) lead to reduced infarct volumina in mouse models of ischemic stroke. Furthermore, our laboratory has shown, that phosphoinositide-3 kinase gamma mediates microglial functions after LPS-preconditioning. Hence, the aim of this work was to characterize proteomic alterations in microglia with (I) ischemic stroke in general in the tMCAO (transient middle cerebral artery occlusion) mouse model of ischemic stroke, (II) the influence of LPS-preconditioning on microglial proteomic alterations after tMCAO and (III) the role of PI3Ky in the microglial proteomic changes after tMCAO and preconditioning. This was done by a single LPS injection 3 days before tMCAO in wildtype mice and mice with PI3Ky knockout or knockin of the kinase dead form of PI3Ky.

2024-03-22 | PXD031930 | Pride

Microglia transcriptome in a rat model of ischemic stroke

Project description:Microglia are key regulators of inflammatory response after stroke and brain injury. Here we profiled the microglia transcriptome isolated from a spontaneously hypertensive rat model of focal cerebral ischemia. We identified an extensive and persistent upregulation of anti-inflammatory M2-like patterns after stroke and a mild up-regulation of pro-inflammatory M1-like patterns at later stage. We also found that younger brains showed larger microglial response than middle aged brains. Moreover, beyond the standard M1/M2 dichotomy, a wide spectrum of novel microglial polarization states was activated in response to stroke, particularly the phenotypes related to Tlr2 and dietary fatty acids stimulation.

2020-04-24 | GSE148350 | GEO

Regulatory T Cell-Microglia Crosstalk Promotes White Matter Repair after Ischemic Stroke through Osteopontin [scRNA-seq]

Project description:CD45high infiltrating immune cells were sorted from ischemic mouse brains at 5 days (5d) and 14 days (14d) after transient (60 min) middle cerebral artery occlusion (tMCAO) and subjected to scRNAseq.

2021-05-19 | GSE171169 | GEO

Single-Cell Analysis Uncovers Dramatic Alteration of Microglia Heterogeneity after Ischemic Stroke

Project description:Microglia are resident myeloid cells in the central nervous system (CNS) that regulate homeostasis and protect CNS from damage and infection. The phenotype of microglia is critical in regulating the propagation and resolution of inflammatory responses after ischemic stroke. However, little is known of its complexity and heterogeneity in the above context. Here, using single-cell RNA sequencing (scRNA-seq) of over 11,000 cells from the mice ischemic brain tissues, we demonstrated a previously undefined molecular heterogeneity among microglia clusters following ischemic stroke.

2023-06-14 | GSE210986 | GEO

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