Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome Analysis of Synovial CD14+ cells in Rheumatoid Arthritis Patients

ABSTRACT: To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. In this dataset, we sought for functional SE-eRNAs in RA patients' synovial monocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE203357 | GEO | 2022/11/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Investigation of Genomic RNA Polymerase II-Rich Locations in Osteoclast Precursor Cells

2022-11-01 | GSE203355 | GEO

Chromatin Accessibility Profiling of Osteoclasts Precursor Cells

2022-11-01 | GSE203354 | GEO

Strand-Specific Nuclear Transcriptome Analysis of Osteoclast Precursor Cells

Project description:To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. In this dataset, we validated the presence of the predicted SE-eRNAs.

2022-11-01 | GSE203359 | GEO

Assessment of genomic location of acetylation of lysine 27 of histone H3 in Osteoclast Precursor Cells [ChIP_seq_H3K27ac]

Project description:To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. This dataset represent histone modification encoding active enhancers genome-wide.

2022-11-01 | GSE203586 | GEO

Base-Level Resolution Run-On Sequencing in Osteoclast Precursor Cells

Project description:To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. This dataset contains precision run-on sequencing (PRO-seq) data performed to detect SE-eRNA transcription activity.

2022-11-01 | GSE203356 | GEO

miR-548aj-3p and miR-3127-3p suppress RANKL-facilitated inflammatory cytokines and catabolic factor in osteoarthritis and rheumatoid arthritis

Project description:Osteoarthritis (OA) and rheumatoid arthritis (RA) are high prevalent joint diseases in global. The common pathological features include synovial inflammation, swelling, joint destruction, and bone remodelling. Arthritis development is associated with joint inflammation, particularly in inflamed synovial cells. Synovial inflammation, driven by cytokines such as interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), is a crucial factor in arthritis as it contributes to joint destruction. RANKL is a vital factor that is linked to the activity of osteoclasts and the erosion of bone. Increased levels of RANKL related with the proinflammatory cytokines and cartilage degradation enzymes expression, playing a role in the course of arthritis. Medicines for arthritis have been limited by side effects and individual variability in therapeutic response. More effective treatment and drug options are needed to improve disease progression. miRNAs directly modulate gene transcription as potential option for arthritis therapeutic. Our study revealed that RANKL stimulation in OA and RA synovial fibroblasts upregulated the expression of IL-1β, IL-6 (pro-inflammatory cytokines) and MMP-13 (catabolic factor) by suppressing miR-548aj-3p and miR-3127-3p. Administration of miR-548aj-3p and miR-3127-3p mimics substantially inhibited the expression of IL-1β, IL-6 and MMP-13. We propose a potentially efficacious miRNA therapeutic approach for the treatment of arthritis, with a specific focus on OA and RA.

2025-11-30 | GSE281545 | GEO

Synovial microenvironment-influenced mast cells promote the progression of rheumatoid arthritis

Project description:Mast cells are phenotypically and functionally highly heterogeneous, and their state is possibly controlled by their local microenvironment. Therefore, concrete analyses are needed to understand whether mast cells act as powerful motivators or dispensable bystanders in specific diseases. Here, we evaluated the correlation between synovial mast cells and rheumatoid arthritis (RA) disease severity, and the efficacy of therapeutic interventions against mast cells. We showed that degranulation of mast cells in inflammatory synovial tissues of RA patients was induced via MAS-related G protein-coupled receptor X2 (MRGPRX2), and the expression of MHC class II (MHC II) and costimulatory molecules on mast cells were upregulated. These unique signaling response led to mast cell activation and promoted T cell responses, resulting in the progression of RA. Collagen-induced arthritis mouse models treated with a combination of anti-IL-17A and cromolyn sodium, a mast cell membrane stabilizer, showed significantly reduced clinical severity and decreased bone erosion. The findings of the present study suggest that synovial microenvironment-influenced mast cells contribute to RA and may provide a novel mast cell-targeting therapy for RA.

2024-01-07 | PXD038584 | Pride

Transcriptomic characterization of classical monocytes highlights the involvement of immuno-inflammation in bone erosion in Rheumatoid Arthritis

Project description:Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with localized bone involvement characterized by the presence of bone erosions. Evidence-based data suggest that under inflammatory conditions, classical monocytes are the main source of osteoclasts and might be involved in bone erosion pathophysiology. Here, we analyze the transcriptomic profile of classical monocytes in erosive and non-erosive rheumatoid arthritis patients in order to better understand their contribution to bone erosion. Thirty-nine premenopausal RA patients and 20 healthy age-matched women were recruited for this study. Classical monocytes were isolated from peripheral blood through negative selection. Sequencing library was constructed using the Quant-seq® 30 mRNA-Seq Library Prep Kit (Lexogen®) and sequenced using an Illumina Seq 2500 platform (Illumina®). Differential expression analysis was performed between patients and control groups. Therefore, gene sets analysis was performed to identify the enriched biological pathways. Results suggested that alterations in pathways related to the inflammatory process and impairment of bone formation have an important role in the pathophysiology of bone erosions in patients with rheumatoid arthritis.

2023-09-19 | E-MTAB-13361 | biostudies-arrayexpress

Impaired ATM Activation in B Cells Promotes Osteoclastogenic Cytokine Production and Bone Erosion in Patients with Rheumatoid Arthritis

Project description:Rheumatoid arthritis (RA) patients may display atypical CD21-/lo B cells in their blood but the significance of this observation remains unclear. We report here that the group of RA patients with elevated frequencies of CD21-/lo B cells shows decreased ataxia-telangiectasia mutated (ATM) expression and activation in B cells compared with other RA patients and healthy donor controls. In agreement with ATM involvement in the regulation of V(D)J recombination, RA patients with defective ATM function displayed a skewed B cell receptor (BCR) Igk repertoire, which resembled that of ataxia-telangiectasia (AT) patients. This repertoire was characterized by increased Jk1 and decreased upstream Vk gene segment usage, suggesting improper secondary recombination processes and selection. In addition, altered ATM function in B cells was associated with decreased osteoprotegerin (OPG) and increased RANKL production. These changes favor bone loss and correlated with a higher prevalence of erosive disease in RA patients with impaired ATM function. Using a humanized mouse model, we also show that ATM inhibition in vivo induces an altered Igk repertoire and RANKL production by immature B cells in the bone marrow, leading to decreased bone density. We conclude that dysregulated ATM function in B cells promotes bone erosion and the emergence of circulating CD21-/lo B cells, thereby contributing to RA pathophysiology.

2019-11-23 | GSE132832 | GEO

Tex10 Coordinates Epigenetic Control of Super-Enhancer Activity for Pluripotency and Reprogramming [ChIP-Seq]

Project description:Super-enhancers (SEs) are large clusters of transcriptional enhancers that are co-occupied by multiple lineage specific transcription factors driving expression of genes that define cell identity. In embryonic stem cells (ESCs), SEs are highly enriched for Oct4, Sox2, and Nanog in the enhanceosome assembly and express enhancer RNAs (eRNAs). We sought to dissect the molecular control mechanism of SE activity and eRNA transcription for pluripotency and reprogramming. Starting from a protein interaction network surrounding Sox2, a key pluripotency and reprogramming factor that guides the ESC-specific enhanceosome assembly and orchestrates the hierarchical transcriptional activation during the final stage of reprogramming, we discovered Tex10 as a novel pluripotency factor that is evolutionally conserved and functionally significant in ESC self-renewal, early embryo development, and reprogramming. Tex10 is enriched at SEs in a Sox2-dependent manner and coordinates histone acetylation and DNA demethylation of SEs. Our study sheds new light on epigenetic control of SE activity for cell fate determination. Genome binding/occupancy profiling of Tex10 was performed in mouse embryonic stem cells by ChIP sequencing.

2015-05-07 | E-GEOD-66735 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data