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Oligodendroglial precursors orchestrate immune cellular network instigating multiple sclerosis

ABSTRACT: Oligodendroglial precursors orchestrate immune cellular network instigating multiple sclerosis

PROVIDER: PRJNA1023979 | ENA |

REPOSITORIES: ENA

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Oligodendroglial precursors orchestrate immune cellular network instigating multiple sclerosis

Project description:The immunomodulatory cellular network that triggers early inflammation and demyelination, the key steps in multiple sclerosis (MS) pathogenesis remains poorly characterized. Here, we demonstrate that overactivation of the Wnt pathway promotes pathological transformation of oligodendrocyte precursor cells (OPCs) to replicate pathological OPCs in human MS. In mouse experimental autoimmune encephalomyelitis (EAE), pathological OPCs attract CD4+ T-helper 1 (Th1) cells into the spinal cord and the brain through CC-chemokine ligand 4 (CCL4). Th1 cells cooperate with OPCs inducing subpopulation of cytotoxic macrophages that execute early demyelination. Simultaneously, Th1 cells and cytotoxic macrophages upregulate Wnt signaling and CCL4 expression in OPCs, thus exerting positive feedback onto the OPC-immune cascade and establishing a vicious cycle propagating EAE pathogenesis. Breaking this cascade by targeting CCL4 reduces immune cell infiltration, alleviates demyelination, and attenuates EAE severity. Our findings demonstrate a closely coordinated network of OPCs and immune cells therefore providing an alternative insight into MS pathophysiology

2025-02-01 | GSE244660 | GEO

Extrinsic inflammatory, but not intrinsic oligodendroglial factors contribute to oligodendroglial differentiation block in multiple sclerosis

Project description:Multiple sclerosis (MS) is the most frequent demyelinating disease and despite significant advances in the immunotherapy, disease progression still cannot be prevented. Promotion of remyelination, an endogenous repair process, represents a promising new treatment approach. However, spontaneous remyelination frequently fails in MS lesions due to an impaired differentiation of progenitor cells into mature, myelinating oligodendrocytes. Intrinsic oligodendroglial and extrinsic inflammatory factors may contribute to this differentiation block. Therefore, we compared induced pluripotent stem cell (iPSC)-derived oligodendrocytes (hiOL) from MS patients and healthy controls as well as their response to extrinsic factors. While functional capabilities or proteome compostion of both cell types were virtually indistinguishable, we discovered that Interferon-gamma (IFNÎ³) producing immune cells significantly impaired oligodendroglial differentiation and observed no differences in the functional capabilities or the proteome. In summary, these data indicate that the oligodendroglial differentiation block is not due to intrinsic oligodendroglial factors, but rather caused by the inflammatory environment present in MS lesions. These findings may contribute to the development of remyelination promoting strategies in MS.

2020-09-04 | PXD016043 | Pride

Progressive multiple sclerosis

Project description:Progressive multiple sclerosis

| PRJNA966951 | ENA

Multiple Sclerosis

Project description:Elevated genetic risk for multiple sclerosis originated in Steppe Pastoralist populations

| PRJEB65098 | ENA

Multiple sclerosis and EAE

Project description:Multiple sclerosis and EAE

| PRJNA391342 | ENA

Transcription signature of Multiple Sclerosis

Project description:This SuperSeries is composed of the following subset Series: GSE17393: Transcription signature of Multiple Sclerosis in peripheral blood mononuclear cells. GSE17409: Pregnancy changes expression in peripheral blood mononuclear cells of healthy donors GSE17410: Pregnancy changes expression in peripheral blood mononuclear cells of Multiple Sclerosis (MS) patients Refer to individual Series

2010-01-10 | E-GEOD-17449 | biostudies-arrayexpress

Neuronal Methylome in Multiple Sclerosis

Project description:Neuronal Methylome in Multiple Sclerosis

| PRJNA489474 | ENA

Imaging Neurodegeneration in Multiple Sclerosis

Project description:Imaging Neurodegeneration in Multiple Sclerosis

| PRJNA827227 | ENA

Molecular cause of the differential activity of Sox8 and Sox10 in oligodendroglial cells

Project description:Oligodendroglial cells are responsible for the generation of myelin sheaths in the central nervous system and thereby render rapid saltatory conduction possible. During development, oligodendroglial cells express the three paralogous transcription factors Sox8, Sox9 and Sox10. In mature oligodendrocytes Sox8 and Sox10 expression persists. Whereas Sox9 and Sox10 fulfill important regulatory roles in these cells, Sox8 has only a limited impact on oligodendroglial development and myelination. By replacing Sox10 with Sox8 or Sox9 in the oligodendroglial Oln93 cell line and by comparing expression profiles, we show that Sox8 regulates the same processes as Sox10 and Sox9, but has a substantially lower transcriptional activity under standard culture conditions.

2025-01-02 | GSE280389 | GEO

Expression data from oligodendroglial cell line

Project description:Coexpression of alpha-synuclein and p25alpha in an oligodendroglial cell line elicites a degenerative response that relies on aggregation and phosphorylation of alpha-synuclein at Ser129 We used microarray analysis to detail the changes in gene expression caused by alpha-synuclein aggregation followed by cellular degeneration Alpha-synuclein was coexpressed with p25alpha in an oligodendroglial cell line and mRNA was isolated at 8, 12, and 16 hrs after transfection. Gene expression was analyzed by two identical microarray set-ups

2013-10-28 | E-GEOD-51781 | biostudies-arrayexpress

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