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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

ABSTRACT: CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

PROVIDER: PRJNA1193576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31588421_1.fastq.gz	Fastqsanger.gz
	SRR31588421_2.fastq.gz	Fastqsanger.gz
	SRR31588422_1.fastq.gz	Fastqsanger.gz
	SRR31588422_2.fastq.gz	Fastqsanger.gz
	SRR31588427_1.fastq.gz	Fastqsanger.gz

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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

Project description:Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. Here, in a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene (CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with mitochodrial, metabolic and multiomic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocyte-specific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathological responses and a candidate therapeutic target in MS. Scheduled for publication in Nature Neuroscience DOI: 10.1038/s41593-025-01875-9

2024-12-03 | GSE283395 | GEO

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

Project description:CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

| PRJNA781235 | ENA

CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

2023-11-09 | GSE189030 | GEO

Project description:The pupose of this study is to explore the mitophagy related transcriptome profiling of the astrocytes differentiated from POLG patient iPSCs compared to the astrocytes generated from healthy control iPSCs.

2021-03-09 | GSE168518 | GEO

Astrocyte-produced HB-EGF limits autoimmune CNS pathology

Project description:Astrocyte-produced HB-EGF limits autoimmune CNS pathology

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Disease-associated astrocyte epigenetic memory promotes CNS pathology [sgEp300, sgACLY astrocytes bulk RNA-Seq dataset]

Project description:Disease-associated astrocyte subsets contribute to the pathology of neurologic diseases, including multiple sclerosis and experimental autoimmune encephalomyelitis1,2,3,4,5,6,7,8 (EAE), an experimental model for multiple sclerosis. However, little is known about the stability of these astrocyte subsets and their ability to integrate past stimulation events. Here we report the identification of an epigenetically controlled memory astrocyte subset that exhibits exacerbated pro-inflammatory responses upon rechallenge. Specifically, using a combination of single-cell RNA sequencing, assay for transposase-accessible chromatin with sequencing, chromatin immunoprecipitation with sequencing, focused interrogation of cells by nucleic acid detection and sequencing, and cell-specific in vivo CRISPR–Cas9-based genetic perturbation studies we established that astrocyte memory is controlled by the metabolic enzyme ATP-citrate lyase (ACLY), which produces acetyl coenzyme A (acetyl-CoA) that is used by histone acetyltransferase p300 to control chromatin accessibility. The number of ACLY+p300+ memory astrocytes is increased in acute and chronic EAE models, and their genetic inactivation ameliorated EAE. We also detected the pro-inflammatory memory phenotype in human astrocytes in vitro; single-cell RNA sequencing and immunohistochemistry studies detected increased numbers of ACLY+p300+ astrocytes in chronic multiple sclerosis lesions. In summary, these studies define an epigenetically controlled memory astrocyte subset that promotes CNS pathology in EAE and, potentially, multiple sclerosis. These findings may guide novel therapeutic approaches for multiple sclerosis and other neurologic diseases.

2025-02-03 | GSE288348 | GEO

Astrocyte-produced HB-EGF limits autoimmune CNS pathology [WGBS]

Project description:Astrocyte-produced HB-EGF limits autoimmune CNS pathology [WGBS]

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RNA-seq and TRAP-seq of astrocytes and brain tissue in mouse models of Alzheimer's pathology

Project description:Alzheimer’s disease is known to alter astrocytes, but the effect of Aß and Tau pathology on these cells remains poorly understood. We investigated the transcriptomic behaviour of astrocytes (via translating ribosome affinity purification (TRAP)), and bulk brain tissue, in mouse models of APP/PS1 ß-amyloidopathy and MAPT-P301S tauopathy, in a mouse model overexpressing cytoprotective Nrf2 specifically in astrocytes (GFAP-Nrf2 model), and in crosses between the amyloidopathy and tauopathy models with the GFAP-Nrf2 mouse.

2021-12-02 | E-MTAB-10985 | biostudies-arrayexpress

Astrocyte-produced HB-EGF limits autoimmune CNS pathology [RNA-Seq]

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APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia

Project description:The major genetic risk factor for Alzheimer’s disease (AD), APOE4, accelerates beta-amyloid (Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or astrocytes is debated. We express here the human APOE isoforms in astrocytes in an Apoe-deficient AD mouse model. This is not only sufficient to restore the amyloid plaque pathology but also induces the characteristic transcriptional pathological responses in Apoe-deficient microglia surrounding the plaques. We find that both APOE4 and the protective APOE2 from astrocytes increase fibrillar plaque deposition, but differentially affect soluble Aβ aggregates. Microglia and astrocytes show specific alterations in function of APOE genotype expressed in astrocytes. Our experiments indicate a central role of the astrocytes in APOE mediated amyloid plaque pathology and in the induction of associated microglia responses.

2024-10-04 | GSE252454 | GEO

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