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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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			Action	DRS
	SRR14097438_1.fastq.gz	Fastqsanger.gz
	SRR14097438_2.fastq.gz	Fastqsanger.gz
	SRR14097439_1.fastq.gz	Fastqsanger.gz
	SRR14097439_2.fastq.gz	Fastqsanger.gz
	SRR14097440_1.fastq.gz	Fastqsanger.gz

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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 [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 [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

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

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

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

Microglia in ischemic brain injury

Project description:Microglia are resident CNS immune cells that are active sensors in healthy brain and versatile effectors under pathological conditions. Cerebral ischemia induces a robust neuroinflammatory response that includes marked changes in the gene expression and phenotypic profile of a variety of endogenous CNS cell types (astrocytes, neurons, microglia) as well as an influx of leukocytic cells (neutrophils, macrophages, T-cells) from the periphery. Many molecules and conditions can trigger a transformation of ârestingâ (or surveying) microglia to an âactivatedâ (alerted/reactive) state. Here we review recent developments in the literature that relate to microglial activation in the experimental setting of in vitro and in vivo ischemia. We also present new data from our own laboratory demonstrating the direct effects of in vitro ischemic conditions on the microglial phenotype and genomic profile. Emphasis is placed on the role of specific molecular signaling systems such as hypoxia inducible factor-1 (HIF-1) and toll-like receptor-4 (TLR4) in regulating the microglial response in this setting. We then review histological and recent novel radiological data that confirms a key role for microglial activation in the setting of ischemic stroke in humans. We discuss recent progress in the pharmacological and molecular targeting of microglia in acute ischemic stroke. Finally, we explore how recent studies on ischemic preconditioning have increased interest in preemptively targeting microglial activation in order to reduce stroke severity. 12 arrays, 4 experimental groups, 3 replicates in each group, CN is control normoxia, CH is control hypoxia, TN is TLR4 knockout normoxia, TH is TLR4 knockout hypoxia.

2010-10-05 | E-GEOD-18602 | biostudies-arrayexpress

Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [RNA-seq]

Project description:The rapid accumulation of self-renewed polarized microglia in the penumbra is the critical neuroinflammatory process after the onset of ischemic stroke, leading to secondary demyelination and neuronal loss. HDAC3 has been reported to regulate cell proliferation of tumour cells and modulate neuroinflammation. However, the mechanism by which HDAC3 regulates microgliosis and microglial polarization remains ambiguous. Herein, we demonstrated that microglia-specific ablation of HDAC3 (HDAC3-miKO) ameliorated poststroke long-term functional and histological outcomes. Starting with unbiased RNA seq of microglia, we identified mitosis as the most significant process reversed by loss of HDAC3. Notably, HDAC3-miKO specifically inhibited the proliferation of M1-like microglia but not M2-like microglia, resulting in microglial transition to an M1-like state. Moreover, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) revealed that HDAC3 deletion induced drastic closing of accessible regions enriched with motifs for PU.1. Taken together, we uncovered for the first time that HDAC3/PU.1-mediated differential proliferation-related reprogramming in different microglia populations drives poststroke inflammatory state transition of microglia and thereby contributes to the pathophysiology of ischemic stroke.

2024-03-13 | GSE220042 | GEO

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