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Expression data from periplaque regions in multiple sclerosis spinal cord

ABSTRACT: There have been few studies that have focused on the periplaque regions surrounding demyelinated plaques, especially in spinal cords. Areas of incomplete demyelination have been demonstrated but poorly studied. The present study aimed to analyze the molecular immunopathology of periplaque demyelinated lesions (PDLs) in the spinal cord of patients with secondary progressive multiple sclerosis (MS). To achieve this goal, the transcriptomic profiles of PDLs were analyzed in post-mortem tissues derived from the cervical spinal cord of 8 patients with primary or secondary progressive MS.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52139 | GEO | 2014/05/30

SECONDARY ACCESSION(S): PRJNA227017

REPOSITORIES: GEO

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Expression data from periplaque regions in multiple sclerosis spinal cord

Project description:There have been few studies that have focused on the periplaque regions surrounding demyelinated plaques, especially in spinal cords. Areas of incomplete demyelination have been demonstrated but poorly studied. The present study aimed to analyze the molecular immunopathology of periplaque demyelinated lesions (PDLs) in the spinal cord of patients with secondary progressive multiple sclerosis (MS). To achieve this goal, the transcriptomic profiles of PDLs were analyzed in post-mortem tissues derived from the cervical spinal cord of 8 patients with primary or secondary progressive MS. Sixteen spinal cord samples were microdissected for RNA extraction and hybridization on Affymetrix microarrays. Eight periplaque samples (P) were compared to normal appearing white matter (N) from the same patient.

2014-05-30 | E-GEOD-52139 | biostudies-arrayexpress

X-linked adrenoleukosdystrophy disease X-ALD

Project description:X-linked adrenoleukodystrophy (X-ALD) is a metabolic genetic disorder of the central nervous system characterized by axonopathy in spinal cords, progressive demyelination in the brain and adrenal insufficiency. Here we provide transcriptomic data from white matter of human X-ALD patients compared to healthy individuals. In particular, from two different disease variants: 1) patients with adrenomyeloneuropathy (AMN) with cerebral demyelination (cAMN) and, 2), an acute, ultimately lethal childhood cerebral form (cALD) featuring severe demyelination in the brain.

2012-03-21 | E-MEXP-3288 | biostudies-arrayexpress

Oxidative damage and respiratory burst in Multiple Sclerosis

Project description:In this project we focused on white matter injury in relapsing remitting MS. We concentrated on material obtained from patients who suffered from fulminant active MS to identify possible sources for ROS production in relation to demyelination and neurodegeneration. To identify possible sources for ROS production in relation to demyelination and neurodegeneration in MS, we used genome wide microarray analysis of gene expression in carefully dissected lesion areas of patients with fulminant acute MS. Preceding the gene expression profiling all cases were characterized histologically and areas of interest were identified. We included 4 control cases, 2 active MS cases were we separated 3 distinct lesions areas (NAWM, initial lesion and early demyelinated lesion) and 1 active MS case were we separated 2 distinct lesion areas (NAWM and early demyelinated lesion). The RNA was isolated from those areas, amplified and hybridized to Agilent G4112A whole genome microarrays.

2011-10-12 | E-GEOD-32915 | biostudies-arrayexpress

Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 1A)

Project description:Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids' saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS. Fig. 1A. Lipid-array profiling of IgG+IgM antibody reactivity in cerebrospinal fluid (CSF) samples from MS patients (relapsing remitting MS; secondary progressive MS; primary progressive MS), healthy controls, and other neurological disease controls. Lipid hits with the lowest FDR (q=0.048) were clustered according to their reactivity profiles. 48 different lipids were custom-spotted in duplicate using the CAMAG Automatic TLC Sampler (ATS4) robot to spray 200 nl of 10 to 100 pmol of lipids onto PVDF membranes affixed to the surface of microscope slides. The slides were probed with cerebrospinal fluid (CSF) from 59 human patient samples. 60 slides total: 18 relapsing-remitting MS, 14 secondary-progressive MS, 1 primary-progressive MS, 21 other neurological disease, 5 healthy control, 1 secondary Ab alone (not included in this submission). CSF diluted 1/10. HRP-conjugated secondary Ab (goat anti-human IgM/IgG) diluted 1/8000. ECL for 3 minutes.

2012-05-08 | E-GEOD-37664 | biostudies-arrayexpress

Epsilon Toxin-Producing Clostridium perfringens within the MS Gut Microbiome and Epsilon Toxin Function on Immune Privilege

Project description:Multiple Sclerosis (MS) is a complex disease of the CNS believed to require one or more environmental triggers and is characterized by episodic formation of inflammatory demyelinating lesions in the brain and spinal cord. Gut dysbiosis is a common feature in MS and here, using enhanced and quantitative PCR detection, we show that people with MS are more likely to harbor and have higher abundance of epsilon toxin (ETX)-producing strains of Clostridium perfringens within their gut microbiome compared to healthy controls (HC). MS patient-derived isolates produce functional ETX and have a genetic architecture typical of highly conjugative plasmids. In the active immunization model of experimental autoimmune encephalomyelitis (EAE), where pertussis toxin (PTX) is used to overcome CNS immune privilege, we find that ETX can substitute for PTX in disease induction. In contrast to PTX-induced EAE, where inflammatory demyelination is largely restricted to the spinal cord, ETX-induced EAE results in multifocal demyelination in the corpus callosum, thalamus, cerebellum, brainstem, and spinal cord, more akin to the lesion distribution observed in MS. Transcriptional profiles from CNS endothelial cells reveal ETX-induced genes that are known to play a role in overcoming CNS immune privilege. Together, these findings support ETX-producing strains of C. perfringens as biologically plausible pathogens in MS to trigger inflammatory demyelination in the context of circulating myelin autoreactive lymphocytes.

2023-03-31 | GSE223137 | GEO

CRISPR-edited human ES-derived oligodendrocyte progenitor cells improve remyelination in rodents

Project description:In Multiple Sclerosis (MS), inflammatory demyelinated lesions in the brain and spinal cord lead to neurodegeneration and progressive disability. Remyelination can restore fast saltatory conduction and neuroprotection but is inefficient in MS especially with increasing age, and is not yet improvable with therapies. Intrinsic and extrinsic inhibition of oligodendrocyte progenitor cell (OPC) function contributes to remyelination failure, and we hypothesised that the transplantation of ‘improved’ OPCs, genetically edited to overcome these obstacles, could improve remyelination. Here, we edited human(h) embryonic stem cell-derived OPCs to be unresponsive to a chemorepellent released from chronic MS lesions, and transplanted them into rodent models of chronic lesions. Edited hOPCs displayed enhanced migration and remyelination compared to controls, regardless of the host age and length of time post-transplant. This study demonstrates that genetic manipulation and transplantation of hOPCs overcomes the negative environment inhibiting remyelination, with translational implications for therapeutic strategies for people with progressive MS.

2023-08-23 | GSE241451 | GEO

Characterisation of Transcriptional Changes in the Spinal Cord of the Progressive Experimental Autoimmune Encephalomyelitis ABH Mouse Model by RNA Sequencing

Project description:RNA sequencing was used to explore global gene expression in the chronic relapsing and secondary progressive EAE (pEAE) Biozzi ABH mouse model of MS. Spinal cord tissue RNA from pEAE Biozzi ABH mice and healthy littermate controls was sequenced. 2,072 genes were differentially expressed (q<0.05) from which 1,397 were significantly upregulated and 675 were significantly downregulated. This hypothesis-free investigation characterised the genomic changes that describe the pEAE mouse model. Examination of 3 control and 3 pEAE mice

2016-07-01 | E-GEOD-78996 | biostudies-arrayexpress

scRNA-seq to examine the reaction of a subpopulation of ependymal cells, EpA cells, to spinal cord injury.

Project description:We performed single cell RNA sequencing to examine the reaction of a subpopulation of ependymal cells, EpA cells, to spinal cord injury. The experiment contains cells from spinal cords of Troy-CreERT2 mice on a Rosa26-tdTomato background. The spinal cord samples come from uninjured and injured spinal cords (3 days after injury).

2022-01-03 | GSE192824 | GEO

Characterisation of Transcriptional Changes in the Spinal Cord of the Progressive Experimental Autoimmune Encephalomyelitis ABH Mouse Model by RNA Sequencing

2016-07-01 | GSE78996 | GEO

Comparative proteomic profiling identifies reciprocal expression of mitochondrial proteins between white and grey matter lesions from multiple sclerosis brains

Project description:Multiple Sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system (CNS), where ongoing demyelination and remyelination failure are the major factors for progressive neurological disability. In this report, we employed a comprehensive proteomic approach and immunohistochemical (IHC) validation to gaininsight into the pathobiological mechanisms that may be associated with the progressive phase of MS disease. Isolated proteins from myelinated regions, demyelinated white matter lesions (WMLs), and grey-matter lesions (GMLs) of well-characterized progressive MS brain tissues were subjected to label-free quantitative mass spectrometry (LFQ-MS). Using a system-biology approach, we detected increased expression of proteins belonging to mitochondrial electron transport complexes and oxidative phosphorylatio pathway in WMLs. Intriguingly, many of these proteins and pathways had opposite expression patterns in GMLs of progressive MS brains. A comparison to the huma MitoCarta database mapped the mitochondrial proteins to mitochondrial subunits in both WMLs and GMLs. Taken together, we provide evidence of opposite expression of mitochondrial proteins in response to demyelination of white- and grey-matter regions in progressive MS brain.

2021-12-21 | PXD029285 | Pride

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