Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392449 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:MicroRNA profiling of demyelination and remyelination areas in corpus callosum of cuprizone-treated mice
| PRJNA392450 | ENA
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
Project description: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.
2018-09-06 | GSE100663 | GEO
Project description:CX3CR1-GFP mice were fed with cuprizone for 4 weeks to induce brain demyelination. The central and lateral parts of the corpus callosum (CC) were then separately dissected, dissociated and GFP+ microglial cells were isolated by FACS. 2133 migroglial cells from medial CC and 2304 cells from lateral CC 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 | GSE144202 | GEO
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
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
Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 6 month old knock-in mice with CAG lengths of 175 along with littermate control wild-type animals. mRNA expression profiles were obtained via RNA-seq analysis performed on samples from the Brown Adipose tissue, White Adipose tissue around Gonad, White Adipose tissue around Intestine, Brain - Brainstem, Brain - Cerebellum, Brain - Hippocampus, Brain - Hypothalamus/Thalamus, Corpus callosum, Gastrocnemius, Heart, and Skin of 6 month old knock-in mice with CAG lengths of 175 along with littermate control wild-type animals.
2016-02-15 | E-GEOD-65775 | biostudies-arrayexpress
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
Project description:Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected fibrinogen-injected corpus callosum to microarray to determine the genes involved in innate and adaptive immune responses by fibrinogen deposited in the CNS after blood-brain barrier disruption. Corpus callosum tissues were isolated from mice received stereotactic injection of fibrinogen or ACSF at 12 hr. Tissues were subjected for RNA extraction and hybridization on Affymatrix microarrays. Two ACSF and two fibrinogen samples were generated.
2015-09-16 | E-GEOD-71082 | biostudies-arrayexpress