Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deep Quantitative Proteomic Profiling of Microglia from the EAE Mouse Model

ABSTRACT: Microglia, the resident immune cells of the central nervous system (CNS), are critically involved in the pathogenesis of multiple sclerosis (MS). To better understand the molecular changes in these cells during neuroinflammation, we performed high-depth quantitative proteomics on microglia isolated from a murine model of MS, experimental autoimmune encephalomyelitis (EAE). This dataset provides a comprehensive proteomic landscape of EAE microglia, offering valuable insights into the cellular mechanisms driving MS pathology.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spinal Cord

SUBMITTER: Jiahong Li

LAB HEAD: Jiahong Li

PROVIDER: PXD067298 | Pride | 2026-06-15

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	MS_identified_information.xlsx	Xlsx
	PXD067298_mzTab.mzTab	Mztab
	Results1.zip	Other
	XB01241B1DA_Acute_EAE_Slot2-42_1_3441.d.zip	Other
	XB01241B1DA_Control_Slot2-41_1_3439.d.zip	Other

Items per page:

1 - 5 of 5

Similar Datasets

Microglia and infiltrating monocytes gene expression profiling during EAE progress

Project description:The project was designed to figure out the role of microglia in brain inflammation (EAE model). The first step was to find genes/pathways that are upregulated in the microglia during EAE progress but absent in the infiltrating monocytes. These genes/pathways may provide clues for studying the unique function of microglia in the brain inflammation that is disctinct from the infiltrating monocytes.

2019-12-05 | GSE133180 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. The top RIPK1 kinase-dependent gene pathways include oxidative phosphorylation and mitochondrial dysfunction in microglia and EIF2 signaling and cholesterol biosynthesis in astrocytes. This study demonstractes critical and distinct roles for RIPK1 kinase signaling in both microglia and astrocytes during EAE

2021-08-12 | GSE154228 | GEO

Quantitative proteomics analysis of liver from LONP1 Knockout mice

Project description:The mechanisms of hepatic stellate cell (HSC) activation and the development of liver fibrosis remains largely unknow. Here, we revealed a fibrosis related mechanism of hepatocytes-HSCs crosstalk regulated by hepatocyte LONP1. We demonstrate that hepatocyte LONP1 expression is decreased in HFD-fed mice and MASH patients. Liver-specific LONP1 deficiency increases orotic acid level and aggravates MASH-induced liver fibrosis in mice. We have identified DHODH as a substrate that is selectively degraded by LONP1 in an ATP-dependent manner. Moreover, activation of LONP1 reduces orotic acid levels and alleviates MASH-induced fibrosis in mice. Mechanistically, LONP1 mediates DHODH turnover, maintaining lower orotic acid levels to inhibit ATF3-mediated HSC proliferation and activation, thereby preventing liver fibrosis. Furthermore, plasma orotic acid levels are negatively correlated with liver LONP1 levels in humans. Therefore, targeting LONP1-mediated hepatocyte-HSC communication may represent a promising therapeutic strategy for MASH-induced liver fibrosis.

2025-09-23 | PXD055467 | Pride

Human Femoral Artery Proteome and 2-Hydroxyisobutyrylation Analysis in Metabolic Syndrome Induced Restenosis

Project description:Restenosis is the primary complication following stenting for coronary and peripheral arterial disease (PAD), posing an ongoing clinical challenge. Metabolic syndrome (MetS), characterized by metabolic disturbances, has been identified as an independent predictor for postoperative restenosis in coronary and carotid arteries, potentially due to endothelial dysfunction and augmented oxidative stress in cells, while its specific regulatory mechanism is still largely unknown. Lysine 2-hydroxyisobutyrylation (Khib), a recently identified post-translational modification, plays a crucial role in transcriptional regulation and cellular metabolism. However, there is a lack of comprehensive analysis of the proteome and Khib modifications within restenotic vessels in the context of MetS, as well as in the understanding of the associated pathophysiology. Here, we firstly validate changes in expression and distribution of Khib in vascular tissues in clinical tissue and cell models. Subsequently, we utilized proteomics and modifiomics to examine the protein and Khib modification characteristics in MetS-induced restenosis.

2025-06-23 | PXD062384 | Pride

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.

2025-06-05 | GSE275400 | GEO

Microarray Sequencing Analysis of microglia from Wild Type and AIM2-/- mice with EAE

Project description:We identified that AIM2 protected against MOG-induced EAE, and AIM2 deficiency in microglia promoted the development of EAE. The purpose of this experiment was to identify how AIM2 protected against MOG-induced EAE.

2020-06-03 | GSE151636 | GEO

Microarray of brain microglia from GM-CSF-expressing B cell conditional knock-out mice at EAE peak stage

Project description:We found a kind of GM-CSF producing B cells (BGM) is positively correlated with the pathogenesis of EAE. BGM cell conditional knock-out (CKO) mice showed significant resistance to EAE. To investigate the relationship between BGM cells and microglia and comprehensively evaluate the status of microglia, we obtained microglia from the brain of CKO and control mice at EAE peak stage, extracted microglial RNA, and performed microarray analysis.

2024-02-25 | GSE167545 | GEO

Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

Project description:To evaluate the potential of EphB3 as a therapeutic target during CNS inflammation, we induced EAE in B6 WT mice and starting at the peak of the disease we initiated treatment with A38 administered. A38 administration ameliorated EAE, and the transcriptional analysis of the astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration.

2022-02-25 | GSE149135 | GEO

Analysis of microglia responses following astrocyte knockdown of interferon gamma signaling during EAE.

Project description:We identify pathways in microglia regulated by astrocyte interferon gamma signaling during EAE

2021-01-09 | GSE154389 | GEO

Transcriptomic profiling of oligodendrocytes, astrocytes, and microglia in an experimental autoimmune encephalomyelitis (EAE) model of demyelination

Project description:The experimental autoimmune encephalomyelitis (EAE) mouse model is widely used to study the pathophysiology of multiple sclerosis (MS), including brain inflammation and demyelination. This study investigates cell-type-specific transcriptional changes in oligodendrocytes, astrocytes, and microglia at day 30 post-induction of EAE using MOG peptide (amino acids 35–55) emulsified in complete Freund’s adjuvant (CFA) containing Mycobacterium tuberculosis, followed by pertussis toxin injections. CFA control mice received only CFA and pertussis toxin, without MOG peptide. Oligodendrocytes, astrocytes, and microglia were isolated using magnetic-activated cell sorting (MACS) from brain and spinal cord of CFA-treated and EAE-induced mice. Bulk RNA sequencing was conducted to uncover transcriptional changes associated with EAE-induced demyelination. These findings will enhance our understanding of glial cell contributions to MS pathogenesis and help identify potential therapeutic targets.

2025-08-17 | GSE287323 | GEO