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Aging-exacerbated demyelinating injury is associated with microglia-derived reactive oxygen species: alleviation by indapamide

ABSTRACT: Aging-exacerbated demyelinating injury is associated with microglia-derived reactive oxygen species: alleviation by indapamide

PROVIDER: PRJNA529670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8799790.fastq.gz	Fastqsanger.gz
	SRR8799791.fastq.gz	Fastqsanger.gz
	SRR8799792.fastq.gz	Fastqsanger.gz
	SRR8799793.fastq.gz	Fastqsanger.gz
	SRR8799794.fastq.gz	Fastqsanger.gz

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Aging-exacerbated demyelinating injury is associated with microglia-derived reactive oxygen species: alleviation by indapamide

Project description:We sequenced the transcriptome of young (6-8 week) and middle-aged (8-10 month old) C57BL/6 female mice that were naïve or had injured ventrolateral spinal cord white matter. We found several differentially expressed genes, many suggesting an altered immune response to injury with advancing age.

2019-03-29 | GSE129000 | GEO

Microglia response upon demyelinating injury [ATAC-seq]

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Microglia response upon demyelinating injury [snRNA-seq]

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Microglia response upon demyelinating injury [ATAC-seq]

Project description:To understand the impaired transcriptional regulation of microglia/macropahges in aging following demyelinating injury. Transcriptional regulation requires the repositioning of the nucleosomes around promoters and enhancers, thereby making chromatin accessible to transcription factors.

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Mitochondrial respiration in microglia is essential for response to demyelinating injury but not proliferation

Project description:Microglia are necessary for CNS function during development and play roles in aging, Alzheimer’s Disease (AD) and the response to demyelinating injury. Mitochondrial respiratory chain (RC) is necessary for conventional T cell proliferation6 and macrophage-dependent immune responses. However, whether mitochondrial RC is essential for microglia proliferation or function is not known. We conditionally deleted the mitochondrial complex III subunit Rieske Iron-Sulfur Protein (RISP) in the microglia of adult mice to assess the requirement of microglial RC for survival, proliferation, and adult CNS function in vivo. Surprisingly, mitochondrial RC function was not required for survival or proliferation of microglia in vivo. RNA-seq analysis showed that loss of RC function in microglia caused changes in gene expression distinct from aged or disease-associated microglia (DAM). Microglia-specific loss of mitochondrial RC function is not sufficient to induce cognitive decline. Amyloid-β plaque coverage decreased and microglial interaction with Amyloid-β plaques increased in the hippocampus of 5xFAD mice with mitochondrial RC-deficient microglia. Microglia-specific loss of mitochondrial RC function did impair remyelination following an acute, reversible demyelinating event. Thus, mitochondrial respiration in microglia is dispensable for proliferation but is essential to maintain a proper response to CNS demyelinating injury.

2024-06-10 | GSE269239 | GEO

Microglia response upon demyelinating injury [snRNA-seq]

Project description:Following demyelinating injury, aged mice have poor recovery compared to young mice. We perforned snRNA seq on the white matter isolated from young and old mice after lesion induction to characterize the transcriptomic signature of glial cells with particular focus on microglia.

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Proteomic and lipidomic profiling of demyelinating lesions identifies fatty acids as modulators in inflammation resolution

Project description:After demyelinating injury of the central nervous system, resolution of the mounting acute innate inflammation is crucial for the initiation of a regenerative response. To identify factors in lesion recovery after demyelination injury, we used a toxin-induced model, in which a single dose of lysolecithin is injected into the corpus callosum to induce a focal demyelinating lesion. Afterwards, we investigated the proteome of demyelinating lesions at different time points post injection (dpi) in a time resolved manner. Lesion sites were excised analyzed from different mice at 0 dpi, without lysolecithin injection, as well as lysolecithin treated mice at 3 dpi, 7 dpi, and 14 dpi. Overall, immune cell migration, especially infiltration of microglia and macrophages, as well as fatty acid metabolism are playing crucial roles for the immidiate response, repair and finally lesion recovery. Additionally, Using lipidomics and eicosanoidomics, we identified bioactive lipids in the resolution phase of inflammation with a marked induction of n-3 polyunsaturated fatty acids. Using fat-1 transgenic mice, which convert n-6 fatty acids to n-3 fatty acids, we found that reduction of the n-6/n-3 ratio facilitates inflammation resolution. In addition, we observed accelerated inflammation resolution and enhanced generation of oligodendrocytes in aged mice when n-3 fatty acids are shuttled to the brain. Thus, n-3 fatty acids and eicosanoids, their oxidized bioactive products, enhance lesion recovery and may therefore provide the basis for novel pro-regenerative medicines of demyelinating diseases in the central nervous system.

2021-09-30 | PXD024891 | Pride

Transcriptional changes in demyelinating canine distemper virus encephalitis

Project description:Canine distemper virus (CDV)-induced demyelinating leukoencephalitis (CDV-DL) in dogs is a translational animal model for human demyelinating diseases such as multiple sclerosis. The aim of this study was to perform an assumption-free microarray analysis of gene expression in different subgroups of CDV-DL as compared to normal controls. Dogs were classified into normal controls (group 1), acute CDV-DL lesions with CDV within the brain but without demyelination and inflammation (group 2), subacute lesions with demyelination but without inflammation (group 3), and subacute to chronic lesions with demyelination and inflammation (group 4).

2014-04-23 | E-MEXP-3917 | biostudies-arrayexpress

Multiple Sclerosis Pattern II Demyelinating Lesions

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Mackinawite nanozymes as reactive oxygen species scavengers for acute kidney injury alleviation.

Project description:BackgroundIron sulfide nanomaterials have been successfully employed as therapeutic agents for bacterial infection therapy and catalytic-ferroptosis synergistic tumor therapy due to their unique structures, physiochemical properties, and biocompatibility. However, biomedical research and understanding of the biological functions of iron sulfides are insufficient, and how iron sulfide nanomaterials affect reactive oxygen species (ROS) in diseases remains unknown. Acute kidney injury (AKI) is associated with high levels of ROS, and therefore nanomedicine-mediated antioxidant therapy has emerged as a novel strategy for its alleviation.ResultsHere, mackinawite nanozymes were synthesized from glutathione (GSH) and iron ions (Fe3+) (denoted as GFeSNs) using a hydrothermal method, and then evaluated as ROS scavengers for ROS-related AKI treatment. GFeSNs showed broad-spectrum ROS scavenging ability through synergistic interactions of multiple enzymes-like and hydrogen polysulfide-releasing properties. Furthermore, both in vitro and in vivo experiments demonstrated that GFeSNs exhibited outstanding cytoprotective effects against ROS-induced damage at extremely low doses and significantly improved treatment outcomes in AKI.ConclusionsGiven the synergetic antioxidant properties and high biocompatibility, GFeSNs exhibit great potential for the treatment of AKI and other ROS-associated diseases.

| S-EPMC10439570 | biostudies-literature

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