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Gene expression profiles from corpus callosum brain tissue obtained from cuprizone-treated mice

ABSTRACT: Mouse cuprizone (CPZ ) model of experimental de- and remyelination was applied to mimic demyelination pathology of multiple sclerosis. The aim of the study was to profile whole genome expression to identify differentially expressed genes during the demyelinisation and after discontinuation of cuprizon treatment, during rapid remyelinisation in affected areas of mouse corpus callosum. Control mice were kept on a normal diet. The following groups representing de- and remyelinisation pathology in corpus callosum of CPZ-treated mice were compared: Partial demyelination: 2weeks CPZ (dem_2w); Complete demyelination: 4weeks CPZ (dem_4w); Remyelination: 4weeks CPZ + UNTREATED (rem); and UNTREATED control (C). The experiments were performed using 3-4 animals per groups.

ORGANISM(S): Mus musculus

PROVIDER: GSE100663 | GEO | 2018/09/06

REPOSITORIES: GEO

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MicroRNA profiling of demyelination and remyelination areas in corpus callosum of cuprizone-treated mice

Project description:Mouse cuprizone (CPZ ) model of experimental de- and remyelination was applied to mimic demyelination pathology of multiple sclerosis. In order to identify differentially expressed microRNAs involved in de- and remyelination, the affected areas of corpus callosum were isolated from mice exposed to CPZ and conducted an Agilent microarray analysis. To induce demyelination, CPZ was administrated for four weeks. Spontaneous remyelination occurs as mice returned to the regular diet after four weeks feeding with CPZ (DEM_4w). Remyelination was examined at two time points: acute remyelination induced by four weeks CPZ feeding followed by two days of regular diet (two days remyelination: REM_2d), and full remyelination induced by four weeks CPZ feeding followed by two weeks of regular diet (two weeks remyelination: REM_2w). Control mice (C) were kept on a normal diet. The following groups representing de- and remyelinisation pathology in corpus callosum of CPZ-treated mice were compared: Demyelination: 4weeks CPZ: DEM_4w; Acute remyelination: 4 weeks CPZ +2 days UNTREATED: REM_2d; Full remyelination: 4 weeks CPZ +2 weeks UNTREATED: REM_2w; and UNTREATED control (C). The experiments were performed using 2-4 animals per groups.

2018-04-11 | GSE100662 | GEO

Multisensory gamma stimulation mitigates the effects of demyelination induced by cuprizone in male mice

Project description:Demyelination is characterized by the loss of the myelin sheath that surrounds nerve fibers and myelin-supporting cells in the nervous system. This leads to increased vulnerability of axons to damage, resulting in significant atrophy and neuro-axonal degeneration. Demyelination is a common pathological feature in a wide range of diseases of the central nervous system (CNS). Multiple pathomolecular processes contribute to brain damage, including demyelination, neuroinflammation, oligodendrocyte (OLs) cell death, and progressive neuronal dysfunction. In this study, we used the cuprizone (CPZ) mouse model to investigate long-term non-invasive gamma entrainment using sensory stimulation (GENUS) as a potential therapeutic intervention for promoting myelination and reducing neuroinflammation. Our results demonstrate that GENUS effectively mitigated demyelination, stimulated oligodendrogenesis in the corpus callosum (CC), and preserved functional integrity and synaptic plasticity. Additionally, GENUS attenuated OLs ferroptosis-induced cell death. Furthermore, chronic GENUS exhibited a marked reduction in brain inflammation, decreasing both microgliosis and astrogliosis and proinflammatory molecules, such as high mobility group box 1 (HMGB1), complement component 1q (C1q) and complement C3 (C3). Considering the pro-remyelination and anti-neuroinflammatory effects observed with GENUS, these findings suggest its potential as a therapeutic approach for demyelinating disorders.

2024-06-07 | GSE240815 | 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

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

Vagus Nerve Stimulation enhances remyelination and decreases innate neuroinflammation in a Multiple Sclerosis rodent model.

Project description:This study investigated the effect of Vagus Nerve Stimulation (VNS) on innate neuroinflammation and remyelination in lysolecithin (LPC) induced demyelination, a preclinical model for Multiple Sclerosis (MS). In a first experiment (demyelination experiment), LPC was injected in the corpus callosum of 33 Lewis rats, inducing a demyelinated lesion, and rats were treated with either continuously-cycled VNS (cVNS) or one-minute per day VNS (1minVNS) or sham VNS, from two days before the injection until three days post-injection (dpi), when they were killed for immunohistochemistry and proteomics analysis. This timepoint corresponded with a demyelinated lesion and peak inflammation. In a second experiment (remyelination experiment), 13 rats were analogously treated with either cVNS or sham from two days before LPC injection until 11 dpi, when they were killed for tissue prelevation for immunohistochemistry and proteomics. This timepoints corresponded with partial remyelination of the lesion. For proteomics analysis, 20 rats were randomly selected, namely five cVNS and five sham rats of the demyelination experiment, and five cVNS and five sham rats of the remyelination experiment.

2024-05-10 | PXD050858 | Pride

Sequencing of microglia during focal remyelination of the corpus callosum

Project description:Sequencing of microglia during focal remyelination of the corpus callosum

| PRJNA485693 | ENA

Single-cell RNA-seq analysis of subventricular zone-derived neural progenitors mobilized to demyelinated corpus callosum

Project description:NestinCreERT2:RosaYFP mice were fed with cuprizone for 4 weeks to induce brain demyelination. Corpus callosum was then dissected, dissociated and YFP+ subventricular zone-derived cells were isolated by FACS. 1931 cells were then processed for single-cell RNA-seq analysis. Single Cell RNA sequencing library were generated using the 10x Genomics Chromium Platform and sequenced on the Illumina Nextseq 500.

2021-06-04 | GSE144201 | GEO

Bulk RNAseq of AnnexinV+ and AnnexinV- cells from the Mertk-KO corpus callosum at the 4 week cuprizone timepoint

Project description:Purpose: Following 4 weeks of 0.2% cuprizone treatment, Mertk-KO mice accumulate dying cells in the corpus callosum (based on cleaved-cas3 staining). These cells are not seen in Mertk-WT animals at the same cuprizone timepoint. The goal of this study is to identify these dying cells in the Mertk-KO corpus callosum Methods: 2 biological replicates (mice) were used. Corpus callosa were dissected from Mertk-KO mice after 4 weeks of 0.2% cuprizone treatment. Tissues were dissected into single cells using Miltenyi Neural Tissue Dissociation Kit (P) and stained with Annexin V. The stained cell suspensions were then FAC sorted into Annexin V+ and Annexin V- populations. RNA from these cells were extracted using QIAGEN RNeasy kit. Results: Bulk RNA-Seq data were analyzed using an in-house pipeline consisting of GSNAP HTSeqGenie. Reads aligning uniquely to exons were counted to each gene, and size-factor normalization was used to calculating nRPKM statistic. Conclusions: Based on the differences of transcriptomic profiles of AnnexinV+ and AnnexinV- cells, we conclude that the dying AnnexinV+ cells are microglia.

2021-04-13 | GSE148677 | GEO

Proteome dynamics during postnatal mouse corpus callosum development

Project description:Formation of cortical connections requires the precise coordination of several discrete stages. This is particularly significant with regard to the corpus callosum, the largest white matter structure bridging both cerebral hemispheres, whose development undergoes several dynamic stages including the crossing of axon projections, the elimination of exuberant projections, and the myelination of established tracts. To comprehensively characterize the molecular events in this dynamic process, we set to determine the distinct temporal expression of proteins regulating the formation of the corpus callosum and their respective developmental functions. Mass spectrometry-based proteomic profiling was performed on early postnatal mouse corpus callosi, for which limited evidence has been obtained previously, using stable isotope of labeled amino acids in mammals (SILAM). The analyzed corpus callosi had distinct proteomic profiles depending on age, indicating rapid progression of specific molecular events during this period. The proteomic expression profiles were then segregated into five separate protein clusters, each with distinct trajectories relevant to their intended developmental functions. Our analysis both confirms many previously-identified proteins in aspects of corpus callosum development, and identifies new candidates in understudied areas of development including callosal axon refinement. We present a valuable resource for identifying new proteins integral to corpus callosum development that will provide new insights into the development and diseases afflicting this structure.

2017-03-29 | PXD005271 | Pride

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