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Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

ABSTRACT: Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

PROVIDER: PRJNA992459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25193012_1.fastq.gz	Fastqsanger.gz
	SRR25193012_2.fastq.gz	Fastqsanger.gz
	SRR25193013_1.fastq.gz	Fastqsanger.gz
	SRR25193013_2.fastq.gz	Fastqsanger.gz
	SRR25193014_1.fastq.gz	Fastqsanger.gz

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Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination

Project description:Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination

| PRJNA993135 | ENA

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

Project description:Demyelination and dysregulated myelination in the CNS are hallmarks of many neurodegenerative diseases such as multiple sclerosis (MS) and leukodystrophies. Here, we studied GFAP+ astrocytes during de- and remyelination in the cuprizone mouse by exploiting the ribosomal tagging (RiboTag) technology. Analyses were performed 5 weeks after cuprizone feeding, at the peak of demyelination in the corpus callosum, and 0.5 and 2 weeks after cuprizone withdrawal, when remyelination and tissue repair is initiated. After 5 weeks of cuprizone feeding, reactive astrocytes showed inflammatory signatures with enhanced expression of genes that modulate leukocyte migration (Tlr2, Cd86, Parp14,Cxcl10). Furthermore, demyelination-induced reactive astrocytes expressed numerous ligands including Cx3cl1, Csf1, Il34, and Gas6 that act on homeostatic as well as activated microglia and thus potentially mediate activation and recruitment of microglia as well as enhancement of their phagocytosis. During early remyelination, region-specific astrocytes displayed reduced inflammatory response signatures as indicated by shut down of CXCL10 production. During late remyelination, the signatures of GFAP+ astrocytes shifted towards resolving inflammation by active suppression of lymphocyte activation and differentiation and support of glia cell differentiation. Astrocytes showed enhanced expression of osteopontin (SPP1) as well as of factors that are relevant for tissue remodelling (Timp1), regeneration and axonal repair. In conclusion, we detected highly dynamic astroglial transcriptomic signatures in the cuprizone model, which reflects excessive communication amongst glia cells and highlights different astrocyte functions during neurodegeneration and regeneration.

2023-07-11 | GSE236805 | GEO

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq I]

2023-07-11 | GSE233951 | GEO

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq I]

Project description:Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq I]

| PRJNA978634 | ENA

Expression data from WT and TREM2 deficient microglia in response to cuprizone mediated demyelination

Project description:We examined the role of TREM2 on microglia responses to demyelination Microglia were FACS-purified from WT or Trem2-/- mice fed with 0.2% cuprizone diet.

2015-04-22 | E-GEOD-66926 | biostudies-arrayexpress

Gene expression profile in the cuprizone-induced demyelination mouse model

2019-03-30 | GSE129049 | GEO

Expression data from white matter astrocytes of wild-type or GnT-IX-deficient mice after cuprizone administration

Project description:Multiple sclerosis (MS) is an immune-based demyelinating disease. Currently available therapeutics target inflammation but have little impact on promoting remyelination. Furthermore, MS diagnosis is sometimes challenging. Using a demyelination model mice, we previously found that protein tyrosine phosphatase receptor type zeta (PTPRZ) receives abnormal glycosylation, a branched O-mannosyl (O-Man) glycan and that branched O-Man glycosylated PTPRZ specifically occurs in reactive astrocytes of demyelinated lesions. Furthermore, by genetically deleting the branching enzyme, GnT-IX (also known as GnT-Vb), astrogliosis was attenuated and remyelination enhanced. To characterize the PTPRZ expressing astrocytes, microarray analysis was performed using astrocytes from mice after short and long term-cuprizone administration.

2023-07-17 | GSE134372 | GEO

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-11 | GSE236929 | GEO

MicroRNA expression in the cuprizone-induced demyelination mouse model

Project description:Myelin abnormalities, oligodendrocyte damage, and concomitant glia activation are common in demyelinating diseases of the central nervous system (CNS). The neurotoxicant cuprizone (CPZ) has been extensively used to create a mouse model of demyelination. However, the changes of miRNA expression and effects on behavior of cuprizone treatment have not been clearly reported. We have analyzed the behavioral changes of mice given a diet containing 0.2% cuprizone for 6 weeks. To evaluate the changes of miRNA expression in CPZ-induced demyelination compared with control, we performed the Affymetrix GeneChip® miRNA 4.0 Array. We identified 1348 and 1253 differentially expressed miRNAs for control and CPZ-treated mice, respectively. Furthermore, the expression of 240 miRNAs was significantly changed in CPZ-induced mice comparing with control mice. These results suggest that the changes of miRNA expression in vivo may provide a new potential remyelination therapeutic target.

2018-11-22 | GSE122839 | GEO

Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance

Project description:How microglia respond and regulate demyelination is not fully understood. To understand how microglia respond during demyelination, we fed mice cuprizone and assessed the response of genetically fate-mapped microglia. Cuprizone-induced demyelination generated a robust microglial response. We conducted single-cell RNA sequencing and identified several cuprizone-associated microglia (CAM) clusters during demyelination. These clusters expressed a transcriptomic signature indicative of cytokine regulation and reactive oxygen species production with altered lysosomal and metabolic changes consistent with ongoing phagocytosis. To understand how microglia contribute to the clearance of dead oligodendrocytes, we ablated microglia starting at the peak of cell death. We used the viability dye acridine orange and monitored apoptotic and lytic cell morphologies after microglial ablation and found that microglia preferentially phagocytose lytic carcasses. In culture, microglia exposed to lytic carcasses partially recapitulated the CAM state, suggesting that phagocytosis contributes to this distinct microglial state during cuprizone demyelination.

2022-08-08 | GSE207570 | GEO

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