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Microglial aryl hydrocarbon receptor enhances phagocytic function and promotes remyelination in a model of multiple sclerosis

ABSTRACT: Microglial aryl hydrocarbon receptor enhances phagocytic function and promotes remyelination in a model of multiple sclerosis

PROVIDER: PRJNA864046 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20723836_1.fastq.gz	Fastqsanger.gz
	SRR20723836_2.fastq.gz	Fastqsanger.gz
	SRR20723837_1.fastq.gz	Fastqsanger.gz
	SRR20723837_2.fastq.gz	Fastqsanger.gz
	SRR20723838_1.fastq.gz	Fastqsanger.gz

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Microglial aryl hydrocarbon receptor enhances phagocytic function and promotes remyelination in a model of multiple sclerosis

Project description:We employed a cuprizone-induced demyelinating model to identify the role of AhR in remyelination with microglial AhR-deficient mice and wild type mice. RNA-seq was performed to compare gene transcriptional profile in wild type mice and microglial AhR-deficient mice of cuprizone model to gain insight into the effects of AhR on microglia function.

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Age-impaired remyelination is associated with dysregulated microglial transitions.

Project description:Multiple sclerosis (MS) is a chronic, inflammatory condition characterized by demyelination and neurodegeneration. Regeneration of lost myelin, or remyelination, occurs in people with MS but is prone to failure and impaired with age. Remyelination is facilitated by microglia but our understanding of the microglial response during remyelination is incomplete. Here, we profiled the microglial response in the lysolecithin mouse model of remyelination using single-cell RNA sequencing. We found several distinct microglial states during the early stages of remyelination that coalesced into a resolved microglial state defined by myelin transcripts. This resolved state was also present in MS brains. As remyelination becomes inefficient with age, we profiled microglia from both young and middle-aged mice during remyelination and found a delay in several microglial states, in concordance with delayed remyelination. Overall, microglia synchronously initiate a multi-faceted response during efficient remyelination in young mice, which becomes dysregulated with age.

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The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

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2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

Microglial aryl hydrocarbon receptor enhances phagocytic function via SYK and promotes remyelination in the cuprizone mouse model of demyelination.

Project description:Multiple sclerosis (MS) is an inflammatory-mediated demyelinating disease of the central nervous system (CNS). Although studies have demonstrated that microglia facilitate remyelination in demyelinating diseases, the underlying mechanisms are still not fully characterized. We found that aryl hydrocarbon receptor (AhR), an environment sensor, was upregulated within the corpus callosum in the cuprizone model of CNS demyelination, and upregulated AhR was mainly confined to microglia. Deletion of AhR in adult microglia inhibited efficient remyelination. Transcriptome analysis using RNA-seq revealed that AhR-deficient microglia displayed impaired gene expression signatures associated with lysosome and phagocytotic pathways. Furthermore, AhR-deficient microglia showed impaired clearance of myelin debris and defected phagocytic capacity. Further investigation of target genes of AhR revealed that spleen tyrosine kinase (SYK) is the downstream effector of AhR and mediated the phagocytic capacity of microglia. Additionally, AhR deficiency in microglia aggravated CNS inflammation during demyelination. Altogether, our study highlights an essential role for AhR in microglial phagocytic function and suggests the therapeutic potential of AhR in demyelinating diseases.

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RNAseq analysis of human CD14+ monocytes exposed to an agonist of Aryl Hydrocarbon Receptor

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Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

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Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.

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