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Corpus callosum bulk RNA sequencing of a cuprizone mouse model of demyelination

ABSTRACT: We used the cuprizone mouse model of multiple sclerosis to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate disease-relevant changes to central nervous system gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE281180 | GEO | 2024/11/08

REPOSITORIES: GEO

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Spinal cord single-nuclei RNA sequencing of an EAE mouse model of multiple sclerosis

Project description:We used the MOG35-55 peptide induction experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate disease-relevant changes to central nervous system gene expression.

2024-11-08 | GSE281176 | GEO

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

Bulk RNA sequencing of primary mouse microglia

Project description:We used primary mouse microglia to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.

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Bulk RNA sequencing of human iPSC-derived microglia

Project description:We used human induced pluripotent stem cell (iPSC)-derived microglia to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.

2024-11-08 | GSE281177 | GEO

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

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

Bulk RNA sequencing of a human iPSC-derived tri-culture

Project description:We used a human induced pluripotent stem cell (iPSC)-derived tri-cultures, comprised of neurons, astrocytes, and microglia, to determine whether Bruton's tyrosine kinase (BTK) inhibition could attenuate differential gene expression induced by Fc receptor stimulation.

2024-11-08 | GSE281178 | GEO

Corpus callosum bulk RNA sequencing of a cuprizone mouse model of demyelination

Project description:Corpus callosum bulk RNA sequencing of a cuprizone mouse model of demyelination

| PRJNA1182681 | ENA

Demyelination and remyelination in anatomically distinct regions of the corpus callosum following cuprizone intoxication.

Project description:Multiple sclerosis is a chronic demyelinating disease of the central nervous system. Spontaneous remyelination during early disease stages is thought to preserve and partially restore function. However, this process ceases in later stages despite the presence of pre-oligodendrocytes. Cuprizone-induced demyelination is a useful model with which to study the remyelination process. Previous studies have demonstrated heterogeneities in demyelination in individual animals. Here we investigated regional differences in demyelination and remyelination within the corpus callosum. C57BL/6 mice were fed 0.2% cuprizone for 5 weeks to induce demyelination. Remyelination was examined 2-5 weeks after cuprizone withdrawal. Immunohistochemistry and electron microscopy were used to quantify regional differences in demyelination, gliosis, and remyelination. We found that, while demyelination was limited in the rostral region of corpus callosum, nearly complete demyelination occurred in the caudal callosum, beginning at approximately -0.5mm from bregma. Astrogliosis and microgliosis were correlated with demyelination and differed between the rostral and caudal callosal structures. Remyelination upon cessation of cuprizone ensued at different rates with splenium remyelinating faster than dorsal hippocampal commissure. Our data show anatomical differences of cuprizone-induced demyelination and remyelination in the corpus callosum and the importance of examining specific callosal regions in myelin repair studies using this model.

| S-EPMC3230728 | biostudies-literature

Affymetrix gene expression of Transitional Type-1 B-cells from Wild-type (CBA), Xid and Btk KO mice

Project description:Splenic Transitional Type-1 B-cells from CBA wild-type mice, X-linked immunodeficiency mice and Bruton's tyrosine kinase knock-out mice. Two replicates where run on Affymetrix 420 2.0 arrays for CBA wild-type, Xid samples and the Btk KO samples. Bruton's tyrosine kinase (Btk) is a cytoplasmic tyrosine kinase important for B-lymphocyte maturation. Mutations in Btk give rise to the primary immunodeficiency disease X-linked agammaglobulinemia (XLA) in man and X-linked immunodeficiency (Xid) in mice. Recent studies have subdivided the mouse immature, or transitional, B-cells into two distinct subsets according to their respective surface markers. Transitional type 1 (T1) and transitional type 2 (T2) cells are also located in distinct anatomic locations. Based on a limited number of markers it has previously been reported that the earliest phenotypic sign of Btk deficiency is manifested at the T2 stage in mice. Here, we report on distinct genome-wide transcriptomic signature differences found in T1 B-lymphocytes from Btk-defective compared to normal mice and demonstrate that Btk deficiency is visible already at this stage. 2 replicates of T1 B-cells from CBA (WT), Xid samples and the Btk KO samples

2014-01-10 | E-GEOD-53946 | biostudies-arrayexpress

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

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