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:Experimental autoimmune encephalomyelitis (EAE) is a key model of autoimmune neuroinflammation, yet an integrated characterization of transcriptional dysregulation in the central nervous system has been limited. In this study, we performed proteomic profiling of dysregulated gene expression in the spinal cord of female and male C57BL/6JRccHsd mice induced with EAE during the acute disease phase using TMT LC-MS/MS. The associated transcriptomics dataset (RNA-sequencing analysis of transcriptomic changes in the spinal cord during experimental autoimmune encephalomyelitis) can be found on GEO. We identified extensive upregulation of innate and adaptive immune response signatures alongside downregulation of neuronal, synaptic, and mitochondrial pathways at the transcript level. Comparative analyses revealed broad pathway‑level changes associated with neuroinflammation, while highlighting limitations of transcriptomics alone in capturing alterations related to synaptic and metabolic integrity. This dataset provides a resource for investigating molecular remodeling of the inflamed central nervous system during autoimmune neuroinflammation.
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: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: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:Experimental autoimmune encephalomyelitis (EAE) is a widely used model for studying multiple sclerosis (MS), characterized by inflammation and demyelination in the central nervous system. This study investigates the transcriptional changes in the spinal cord of mice at day 35 post-induction of EAE. Bulk RNA sequencing was performed on spinal cord samples from three groups: (1) naïve mice, (2) mice treated with complete Freund’s adjuvant (CFA) and pertussis toxin (CFA control group), and (3) EAE-induced mice administered MOG peptide (amino acids 35–55) emulsified in CFA with pertussis toxin (MOG group). These findings provide insights into the spinal cord’s transcriptional response during EAE and advance our understanding of MS pathogenesis.
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.
