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Microglia response upon demyelinating injury [snRNA-seq]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE230480 | GEO | 2024/07/24

REPOSITORIES: GEO

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Microglia response upon demyelinating injury [snRNA-seq]

Project description:Microglia response upon demyelinating injury [snRNA-seq]

| PRJNA961192 | ENA

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

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

Temporal transcriptomic profiles of brain regions following acute and chronic demyelinating injury

Project description:Purpose: The central nervous system (CNS) possesses intrinsic remyelination capabilities in response to demyelinating injury. However, this remyelination potential is diminished as demyelinating disease such as multiple sclerosis progresses overtime. To better understand myelin repair processes, the goal of this study was to determine temporal transcriptomic changes in cerebral white matter (corpus callosum) and gray matter (cortex and hippocampus) after acute and chronic demyelinating injury. The cuprizone mouse model of de- and remyelination was used for this investigation. Methods: Adult C57BL/6 mice were exposed to cuprizone diet (0.2%) for 3, 5 or 12 weeks followed by returning to normal diet for up to 12 weeks for recovery. Brain regions were dissected for bulk RNA-seq. Conclusion: RNA-seq analyses suggest common and distinct spatiotemporal transcriptional alterations during CNS demyelination and remyelination. Dataset for this study represents the first that covers gene expression landscapes of three brain regions over extended regenerative periods after chronic CNS demyelination.

2023-04-03 | GSE212147 | GEO

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.

2024-07-24 | GSE230187 | GEO

Microglia response upon demyelinating injury [ATAC-seq]

Project description:Microglia response upon demyelinating injury [ATAC-seq]

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Integrative and comparative single-cell analysis reveals the transcriptomic difference between tumefactive demyelinating lesion and glioma

Project description:Tumefactive demyelinating lesion (TDL) is an immune-mediated disease which could appear like glioma. Here, we perform integrative and comparative single-cell RNA sequencing (ScRNA-seq) transcriptomic analysis on TDL and glioma lesions.

2022-07-28 | GSE202096 | GEO

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

Comparison of cerebrospinal fluid proteomics between Demyelinating disease and non-inflammatory neurological controls

Project description:Demyelinating disease is a disease of the nervous system in which the nerve demyelinating is the main or primary lesion, and the axon, cell body and glia are relatively lightly damaged. It can occur in the central nervous system or the peripheral nervous system. The demyelinating diseases of central nervous system are represented by multiple sclerosis (MS) and neuromyelitis optica (NMO) while Guillain-Barre Syndrome (GBS) is a demyelinating disease of the peripheral nervous system. We aimed to identify the key proteins in demyelinating disease and describe the proteomic pattern of MS, GBS and NMO. This study used high-resolution liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS), in combination with quantitative 10-plex tandem mass tag labeling, to profile protein changes in MS, GBS and NMO.

2020-12-09 | PXD023027 |

Gray but not white matter astroglia-specific connexin 43 ablation ameliorates neuroinflammation [Affymetrix]

Project description:Objective: We previously reported that white matter connexin43 (Cx43) may related to the severity of the multiple sclerosis (MS), whereas the role of gray matter Cx43 in demyelinating disease is unknown. It was considered MS lesions were only exist in white matter, but recent studies revealed that demyelinating lesions are also exist in the cerebral cortex. This fact suggest the possibility that gray matter is somewhat related to the pathophysiology of MS. In this study, we aimed to clarify the role of gray matter Cx43 in a mouse model of MS (experimental autoimmune encephalomyelitis [EAE]). Methods: We developed Cx43F/F;Glutamate aspartate transporter (GLAST)-CreER(T2)KI/+ mice as gray matter specific Cx43 conditional knock-out (Cx43cKO) mice. We induced MOG-EAE 10 days after tamoxifen injection, and analyze its clinical course and pathology. We used Cx43F/F mice as controls. Results: EAE was significantly milder in gray matter astrocyte-specific Cx43cKO mice from acute phase to chronic phase, as compared with control mice. Pathology demonstrated less demyelinating lesions and infiltrating cells. Infiltrating immune cells did not express Cx43 in the active demyelinating lesions of the lumbar cord in both groups. The expression level of Cx43 was similar between these two groups in the spleen and the inguinal lymph nodes. Interpretation: Acute KO of gray matter specific Cx43 before induction of EAE reduce its aggressiveness. This finding may suggest the possibility that gray matter Cx43 modify the MS pathophysiology.

2021-04-20 | GSE148931 | GEO

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