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Deciphering the role of oligodendroglial Serpina3n in EAE pathology using single-cell RNA sequencing

ABSTRACT: Deciphering the role of oligodendroglial Serpina3n in EAE pathology using single-cell RNA sequencing

PROVIDER: PRJNA1212078 | ENA |

REPOSITORIES: ENA

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Deciphering the role of oligodendroglial Serpina3n in EAE pathology using single-cell RNA sequencing

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.

2025-08-17 | GSE287310 | GEO

The impact of oligodendroglial Serpina3n depeletion on brain aging in mice

Project description:This study investigates the role of oligodendroglial Serpina3n in brain aging by examining its depletion using Olig2-Cre Serpina3n flox/flox mice model. To assess the molecular impact of oligodendroglial Serpina3n depletion on brain aging, RNA-seq was performed on forebrain samples from three experimental groups: 1) Young Wild-Type Mice (2-month-old): Representing baseline gene expression in a young, healthy brain; 2) Aged Wild-Type Mice (22-month-old): Serving as a control group to analyze age-related changes in gene expression without genetic modifications. 3) Aged Olig2-Cre Serpina3n flox/flox mice (22-month-old): Assessing the effects of oligodendroglial Serpina3n depletion on the transcriptomic profile of aged brains. The experiment aims to identify gene expression changes associated with normal brain aging by comparing young and aged wild-type mice, determine the specific impact of oligodendroglial Serpina3n depletion on the aged brain by comparing aged wild-type mice to aged knockout mice, and highlight molecular mechanisms influenced by Serpina3n in the context of brain aging. This design allows for a comparative analysis of aging-related transcriptional changes and the specific contribution of Serpina3n depletion in this process.

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The impact of oligodendroglial Serpina3n depeletion on brain aging in mice

Project description:The impact of oligodendroglial Serpina3n depeletion on brain aging in mice

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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

Project description:Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

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Expression data of CNS T cells during EAE

Project description:In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease. We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease. To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2. T cells infiltrating CNS tissues were isolated at peal acute EAE (D18) or during late,chronic EAE (D32). RNA expression was then analysed by genechip to determine the influence of NR4A2 in T cells on these disease stages

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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

Effect of depletion of the serine protease inhibitors (serpina3n) on gene expression in cardiac fibroblasts after myocardial injury (MI) in rodent models

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Brd4 expression in microglia supports microglial activation, T cell recruitment, and demyelination in EAE

Project description:In EAE, a mouse model of multiple sclerosis, immunization with MOG autoantigen results in the generation of Th1/Th17 T cells in the periphery. MOG antigen-specific T cells then invade into the central nervous system (CNS) resulting in neuronal demyelination. Microglia, specialized innate immune cells in the CNS, have been suggested to participate in the pathogenesis of EAE. Bromodomain inhibitors have been reported to reduce EAE pathology by inhibiting T cells. However, the contribution of BRD4 in EAE pathology is unknown. In this study, we demonstrate that microglia-specific Brd4 conditional knockout (cKO) mice, displayed markedly reduced EAE pathology. Brd4cKO microglia failed to express inflammation and activation-related genes and had reduced CNS T cell invasion. Moreover, Brd4cKO microglia: invading T cell interactions were markedly reduced, suggesting that Brd4-dependent microglial genes may play important roles in facilitating T cell restimulation within the CNS. In summary, our results demonstrate a model in which microglial BRD4 plays a key role in supporting neuroinflammation in EAE.

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CRISPR screen identified CLEC16A suppresses astrocyte inflammasome-involved pathology via mitophagy: EAE study

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SerpinA3N limits cartilage destruction in osteoarthritis by inhibiting macrophage-derives leukocyte elastase

Project description:Inflammatory mediators such as interleukin 6 (IL-6) are known to activate catabolic responses in chondrocytes during osteoarthritis (OA). This study aimed to investigate the downstream targets of IL-6 in murine chondrocytes. RNA-sequencing was performed in murine articular chondrocytes treated with IL-6 in hypoxia (1%O2) or normoxia (21%O2). RNA-sequencing revealed that SerpinA3N is a major target of IL-6 in articular chondrocytes. The expression of SerpinA3N was increased in OA cartilage and further investigated.

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