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VDR-dependent signaling modulates neuroinflammation in the acute phase of ischemic stroke

ABSTRACT: VDR-dependent signaling modulates neuroinflammation in the acute phase of ischemic stroke

PROVIDER: PRJNA786209 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17129519_1.fastq.gz	Fastqsanger.gz
	SRR17129519_2.fastq.gz	Fastqsanger.gz
	SRR17129520_1.fastq.gz	Fastqsanger.gz
	SRR17129520_2.fastq.gz	Fastqsanger.gz
	SRR17129521_1.fastq.gz	Fastqsanger.gz

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VDR-dependent signaling modulates neuroinflammation in the acute phase of ischemic stroke

Project description:VDR deficiency in microglia markedly aggravated infarct volumes, neurological deficits, and neuroinflammation after cerebral ischemia. To investigate the role of VDR in microglia-regulated neuroinflammation, we performed RNA-seq analysis on microglia isolated from poststroke microglia-conditional VDR knockout (Vdr-cKO) mice and littermate controls. VDR elimination dramatically alters the gene expression profiles of postischemic microglia, implying that vitamin D signaling play a crucial role in microglia-modulated stroke pathogenesis.

2023-06-21 | GSE190171 | GEO

TRIM9-mediated resolution of neuroinflammation confers neuroprotection against ischemic stroke in mice

Project description:Excessive and unresolved neuroinflammation is part of the pathological cascade in brain injuries such as acute ischemia, as well as neurodegenerative diseases, including multiple sclerosis and Alzheimer’s disease. Particularly, timely resolution of inflammation is critical for the recovery and repair after brain injury. The nuclear factor-κB (NF-κB) signaling plays a central role in neuroinflammation through transcriptional induction of proinflammatory genes. Here, we report that TRIM9, a brain-specific member of the TRIpartite motif (TRIM) family with ubiquitin E3 ligase activity, is upregulated in the peri-infarct cortical areas of mouse brain upon ischemic stroke, and governs the resolution of NF-κB-mediated neuroinflammation. Mechanistically, neuronal TRIM9 sequestered β-TrCP, a component of the Skp-Cullin-F-box (SCF) E3 ligase complex, from ubiquitinating IκBα, thereby mitigating NF-κB-dependent inflammatory responses including production of proinflammatory mediators and infiltration of immune cells. Consequently, Trim9 deficient mice were highly vulnerable to ischemia, manifesting uncontrolled neuroinflammation and exacerbated neuropathological and neurological outcomes. Systemic administration of recombinant adeno-associated virus (AAV)-PHP.B, allowing brain-wide enriched TRIM9 expression, effectively resolved neuroinflammation and alleviated neuronal death in aging mice. This reveals that TRIM9 is essential for fine tuning of NF-κB-dependent neuroinflammation, and TRIM9-potentiation based therapy may offer a new approach for the treatment of stroke and inflammation-related neurological disorders.

2018-12-31 | GSE114652 | GEO

Gene expression analysis of peripheral whole blood RNA following ischemic stroke

Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans. Total RNA extracted from whole blood in n=39 ischemic stroke patients compared to n=24 healthy control subjects.

2010-06-08 | E-GEOD-16561 | biostudies-arrayexpress

TRIM9-mediated resolution of neuroinflammation confers neuroprotection against ischemic stroke in mice

Project description:TRIM9-mediated resolution of neuroinflammation confers neuroprotection against ischemic stroke in mice

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Epigenome analysis of ischemic stroke patients

Project description:We performed a genome-wide methylation study in whole-blood DNA from 404 ischemic stroke patient cohort, distributed across 3 ischemic stroke subtypes: Large-artery atherosclerosis (n=132), Small-artery disease (n=141) and Cardio embolic (n=127) . Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites. We performed a genome-wide methylation study in whole-blood DNA from 185 ischemic stroke patient cohort. Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites.

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Dynamic astrocytic gene expression profiles after ischemic stroke

Project description:Analysis of astrocytic gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying astrocytic activation after ischemic stroke.

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Dynamic microglial gene expression profiles after ischemic stroke

Project description:Analysis of microglial gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying microglial activation after ischemic stroke.

2022-01-01 | GSE172456 | GEO

Gene expression analysis of peripheral whole blood RNA following ischemic stroke

2010-06-01 | GSE16561 | GEO

Effects of Trem2 depletion on gene expressions in a mouse photothrombotic stroke model

Project description:Ischemic stroke is a major threat to public health. Microglia-mediated neuroinflammation is a double-edged sword for neuronal survival after stroke. Triggering receptor expressed on myeloid cells 2 (Trem2) is specifically expressed on the surface of myeloid cell, including microglia. Here, we applied a photothrombotic mouse model of stroke to better understand the role of Trem2 in post-stroke neuroinflammation. In this model, Trem2 was sufficiently induced with sustainably elevated inflammatory responses. Our results demonstrated that Trem2-depletion can ameliorate ischemic injury with enhanced neuronal survival, reduced pro-inflammatory cytokine levels, and improved neurological functions. Our results suggested that Trem2 depletion is neuroprotective during ischemic stroke.

2024-12-29 | GSE280846 | GEO

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2021-03-06 | GSE168383 | GEO

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