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Endothelial cells mediated by STING signaling regulate oligodendrogenesis and myelination during brain development

ABSTRACT: Endothelial cells mediated by STING signaling regulate oligodendrogenesis and myelination during brain development

PROVIDER: PRJNA947569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23940439_1.fastq.gz	Fastqsanger.gz
	SRR23940439_2.fastq.gz	Fastqsanger.gz
	SRR23940440_1.fastq.gz	Fastqsanger.gz
	SRR23940440_2.fastq.gz	Fastqsanger.gz
	SRR23940441_1.fastq.gz	Fastqsanger.gz

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Endothelial cells mediated by STING signaling regulate oligodendrogenesis and myelination during brain development

Project description:To gain futher insight into how endothelial STING regulates oligodendrogenesis ,RNA-seq was used to analyze the genome-wide changes resulting from isolated endothelial cells of E18 endothelial STING conditional knock out mice and littermate wild-type.mRNA from E18 isolated endothelial cells of wild-type(WT) and STINGf/f;Tie2-cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics

2023-03-25 | GSE227955 | GEO

Endothelial Pd1 orchestrates cerebrovasculature homeostasis and oligodendrogenesis during brain development

Project description:Purpose: To explore further into the mechanisms by which endothelial PD1 controls cerebrovascular development and oligodendrogenesis, we employed RNA-seq to examine genome-wide alterations in endothelial cells from P0 conditional PD1 knockout mice, comparing them with their wild-type littermates. Methods: mRNA was extracted from P0 isolated endothelial cells of Pd1fl/fl and Pd1cKO-Tie2 mice, and the quality and quantity were assessed using the Agilent 2100 Bioanalyzer. Subsequently, the mRNA was converted to cDNA and Libraries were prepared. RNA-sequencing was performed on the Illumina HiSeq 2500 platform at Annoroad Genomics. Results: Approximately one thousand transcripts showed differential expression between the Pd11fl/fl and Pd1cKO-Tie2 mice brain endothelial cell, with a fold change ≥2 and p value <0.05.Geneontology analysis of the downregulated genes were enriched in terms related to positive regulation of angiogenesis, positive regulation of vascular endothelial growth factor production and positive regulation of inflammatory response. Concomitantly, upregulated genes were enriched in terms related to endothelial cell migration, sequestering of BMP from receptor via BMP binding and regulation of establishment of blood-brain barrier. These results reflected endothelial PD1 plays vital roles in cortex development. Conclusions: Endothelial PD1 RNA-seq would provide a overall understanding how endothelium-derived PD1regulates vessel development and oligodendrogenesis during brain development

2024-05-13 | GSE267172 | GEO

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [ChIP-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. Examination of Chd7 and Sox10 genomewide occupancy in differentiating oligodendrocytes

2016-02-29 | E-GEOD-72725 | biostudies-arrayexpress

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [RNA-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. 4 RNA-Seq samples from P8 spinal cords of Ctrl and Chd7 cKO mice (duplicatess, Ctrl and cKO)

2016-02-29 | E-GEOD-72726 | biostudies-arrayexpress

Endothelial Pd1 orchestrates cerebrovasculature homeostasis and oligodendrogenesis during brain development

Project description:Endothelial Pd1 orchestrates cerebrovasculature homeostasis and oligodendrogenesis during brain development

| PRJNA1110160 | ENA

A novel STING variant triggers endothelial toxicity and SAVI disease

Project description:Gain-of-function mutations in STING cause STING-associated vasculopathy with onset in infancy (SAVI) characterized by early-onset systemic inflammation, skin vasculopathy, and interstitial lung disease. Here, we report and characterize a novel STING variant (F269S) identified in a SAVI patient. single-cell transcriptomics of patient bone marrow revealed spontaneous activation of interferon (IFN) and inflammatory pathways across cell types and a striking prevalence of circulating naïve T cells was observed. Inducible STING F269S expression conferred enhanced signaling through ligand-independent translocation of the protein to the Golgi, protecting cells from viral infections but preventing their efficient immune priming. Additionally, endothelial cell activation was promoted and further exacerbated by cytokine secretion by SAVI immune cells, resulting in inflammation and endothelial damage. Our findings identify STING F269S mutation as a novel pathogenic variant causing SAVI, highlight the importance of the crosstalk between endothelial and immune cells in the context of lung disease and contribute to a better understanding of how aberrant STING activation can cause pathology.

2024-06-04 | GSE267837 | GEO

Voluntary running triggers VGF-mediated oligodendrogenesis to prolong the lifespan of Snf2h-null ataxic mice

Project description:Exercise enhances cognitive function and slows progressive neurodegenerative disease. While exercise promotes neurogenesis, oligodendrogenesis and adaptive myelination are also significant contributors to brain repair and brain health. Nonetheless, the molecular details underlying these effects remain poorly understood. Conditional ablation of the Snf2h gene (Snf2h cKO) impairs cerebellar development producing mice with poor motor function, progressive ataxia and death between postnatal day 25 to 45. Here we show that voluntary running induced an endogenous brain repair mechanism that resulted in a striking increase in hindbrain myelination and the long-term survival of Snf2h cKO mice. Further experiments identified the VGF growth factor as a major driver underlying this effect. VGF neuropeptides could promote oligodendrogenesis in vitro, while Snf2h cKO mice treated with full-length VGF-encoding adenoviruses obliterated the requirement of exercise for survival. Together, these results suggest that VGF delivery could represent a therapeutic strategy for cerebellar ataxia and other pathologies of the central nervous system.

2016-08-31 | GSE86235 | GEO

Nerve Growth Factor neutralization promotes oligodendrogenesis by increasing miR-219a-5p levels

Project description:Alterations of the crosstalk between the nervous and immune systems may underlie the inflammatory and neurodegenerative changes characterizing Multiple Sclerosis (MS). Among the molecules that actively interconnect these two systems is the Nerve Growth Factor (NGF), involved in both regulating inflammation and in brain homeostasis. Additionally, NGF is known to modulate oligodendrogenesis and reduce myelination, further suggesting an involvement of NGF in MS ethiology. In this study, we find that NGF regulates oligodendrogenesis by modulating the levels of miR-219a-5p, a well-known positive regulator of oligodendrocyte (OL) differentiation. We utilized a transgenic NGF-deprivation mouse model, AD11, in which postnatal expression of an anti-NGF antibody leads to NGF neutralization and progressive neurodegeneration. Notably, we find that these mice also display increased myelination. A microRNA profiling of AD11 brain samples (hippocampus) by Agilent microarray analysis revealed that NGF deprivation leads to an increase of miR-219a-5p levels and a downregulation of its predicted targets, compared to AD11-VH control mice. The AD11-VH controls are transgenic mice where only the heavy chain of the transgenic antibody is expressed, while in AD11 mice express the whole functional antibody (heavy + light chain)

2021-02-15 | GSE162675 | GEO

Endothelial Cell Expression of a STING Gain-of-function Mutation Initiates Pulmonary Lymphocytic Infiltration

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Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [RNA-seq]

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