Project description:Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS); its cause is unknown. To understand the pathogenesis of MS, researchers often use the experimental autoimmune encephalomyelitis (EAE) mouse model. Here, our aim was to build a proteome map of the biological changes that occur during MS at the major onset sites—the brain and the spinal cord. We performed quantitative proteome profiling in five specific brain regions and the spinal cord of EAE and healthy mice with high-resolution mass spectrometry based on tandem mass tags.
Project description:Microarrays were used to identify genes that were differently expressed in mouse spinal cord as a resut of experimental autoimmune encephalomyelitis (EAE), which is a model for demyelinating disease. Mice were injected with PLP peptide or vechicle.
Project description:We have performed transcriptomic analysis in the spinal cord of experimental autoimmune encephalomyelitis (EAE) mice compared to naive mice at different time intervals in order to observe the gene expression changes within the CNS compartment
Project description:In this study, we performed quantitative proteomics utilizing a data-independent acquisition (DIA) strategy to investigate the proteome alteration in the brain and spinal cord tissues from mice with experimental autoimmune encephalomyelitis (EAE), a widely-used model for MS.
Project description:To address the differential response of the CNS, proteomics was applied in experimental autoimmune encephalomyelitis (EAE) mice and cuprizone (CPZ) mice in two different CNS regions
Project description:Microarrays were used to identify genes that were differently expressed in mouse spinal cord as a resut of experimental autoimmune encephalomyelitis (EAE), which is a model for demyelinating disease.
Project description:This study employs single-cell RNA sequencing (scRNA-seq) to investigate cellular and transcriptional changes in the spinal cord at day 27 post-induction of experimental autoimmune encephalomyelitis (EAE). Samples were collected from three groups: (1) control mice treated with CFA only (Ctrl_CFA), (2) EAE-induced mice with MOG peptide administration (Ctrl_MOG), and (3) EAE-induced mice with oligodendrocyte-specific Serpina3n deletion (Olig2-Cre Serpina3n flox/flox, Serpina3n cKO_MOG). This approach aims to dissect the cellular diversity and molecular pathways affected by EAE, with a focus on the role of oligodendroglial Serpina3n in modulating neural cellular function and neuroinflammation. The findings provide insights into cell-specific contributions to spinal cord inflammation and demyelination, highlighting Serpina3n as a potential therapeutic target.
Project description:This file contains gene microarray data from FACS purified mouse memory phenotype CD4+ T cells (CD44hiCD45RBloCD25-), which were isolated from lymph node and spinal cord tissues of mice with experimental autoimmune encephalomyelitis (EAE), a widely studied model of human multiple sclerosis (MS). Memory phenotype CD4+ T cells infiltrating the CNS during EAE expressed high levels of mRNA for Dgat1 encoding diacylglycerol-O-acyltransferase-1 (DGAT1). We studied the biology of DGAT1 in EAE models and in assays of T cell differentiation and function.
Project description:Experimental autoimmune encephalomyelitis (EAE) is a murine model of multiple sclerosis, a chronic neurodegenerative and inflammatory autoimmune condition of the central nervous system (CNS). Pathology is driven by the infiltration of autoreactive CD4+ lymphocytes into the CNS where they attack neuronal sheaths causing ascending paralysis. We used an isotope-coded protein labelling approach to investigate the proteome of CD4+ cells isolated from the spinal cord and brain of mice at various stages of EAE progression in two EAE disease models; PLP139-151-induced relapsing-remitting EAE and MOG35-55-induced chronic EAE, which emulate the two forms of human multiple sclerosis. A total of 1120 proteins were quantified across disease onset, peak-disease and remission phases of disease and of these, 13 up-regulated proteins of interest were identified with functions relating to the regulation of inflammation, leukocyte adhesion and migration, tissue repair and the regulation of transcription/translation. Proteins implicated in processes such as inflammation (S100A4 and S100A9) and tissue repair (Annexin A1), which represent key events during EAE progression were validated by quantitative PCR. This is the first targeted analysis of autoreactive cells purified from the CNS during EAE, highlighting fundamental CD4+ cell-driven processes that occur during the initiation of relapse and remission stages of disease.
