Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via osteoclastgenesis in the joint.

ABSTRACT: Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via osteoclastgenesis in the joint.

PROVIDER: PRJNA1138652 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29912186_1.fastq.gz	Fastqsanger.gz
	SRR29912186_2.fastq.gz	Fastqsanger.gz
	SRR29912187_1.fastq.gz	Fastqsanger.gz
	SRR29912187_2.fastq.gz	Fastqsanger.gz
	SRR29912188_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via osteoclastgenesis in the joint.

Project description:Cellular Communication Network Factor 3 (CCN3) is a secreted protein. It belongs to the CCN family of regulatory proteins, which play essential roles in various cellular processes. In this study, we investigated the functional characteristics of CCN3 in rheumatoid arthritis. We found CCN3 is involved in cellular senescence and osteoclastgenesis of macrophage in vitro. To understand this mechanism, CCN3 is were added to Macrophage and their responses were examined by bulk-RNA analysis.

2024-11-26 | GSE272743 | GEO

Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via promoting cell senescence in synovial cells

Project description:Cellular Communication Network Factor 3 (CCN3) is a secreted protein. It belongs to the CCN family of regulatory proteins, which play essential roles in various cellular processes. In this study, we investigated the functional characteristics of CCN3 in rheumatoid arthritis. We found CCN3 is involved in cellular senescence and inflammation of fibroblast like synoviocyte (FLS) in vitro. To understand this mechanism, CCN3 is were added to FLS and their responses were examined by bulk-RNA analysis.

2024-11-26 | GSE271643 | GEO

Rheumatoid arthritis

Project description:Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease of unknown etiology and pronounced inter-patient heterogeneity. To characterize RA at the molecular level and to uncover key pathomechanisms, we performed whole-genome gene expression analyses. Synovial tissues from rheumatoid arthritis patients were compared to those from osteoarthritis patients and to normal donors. Keywords: disease state analysis

2004-11-04 | GSE1919 | GEO

Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via promoting cell senescence in synovial cells

Project description:Cellular Communication Network Factor 3 contributes to the pathological process of rheumatoid arthritis via promoting cell senescence in synovial cells

| PRJNA1132678 | ENA

Joint-specific DNA transcriptome signatures in rheumatoid arthritis [RNA-seq]

Project description:Stratifying patients on the basis of molecular signatures could facilitate development of therapeutics that target pathways specific to a particular disease or tissue location. Previous studies suggest that pathogenesis of rheumatoid arthritis (RA) is similar in all affected joints. Here we show that distinct DNA methylation and transcriptome signatures not only discriminate RA fibroblast-like synoviocytes (FLS) from osteoarthritis FLS, but also distinguish RA FLS isolated from knees and hips. Using genome-wide methods, we show differences between RA knee and hip FLS in the methylation of genes encoding biological pathways, such as IL-6 signaling via JAK-STAT pathway. Furthermore, differentially expressed genes are identified between knee and hip FLS using RNA-seq. Double-evidenced genes that are both differentially methylated and expressed include multiple HOX genes. Joint-specific DNA signatures suggest that RA disease mechanisms might vary from joint to joint, thus potentially explaining some of the diversity of drug responses in RA patients.

2016-06-09 | GSE80072 | GEO

Joint-specific DNA methylation signatures in rheumatoid arthritis [methylation array]

2016-06-09 | GSE80071 | GEO

Expression data from Rheumatoid Arthritis synovial tissue samples

Project description:Rheumatoid arthritis (RA) is a complex and clinically heterogeneous autoimmune disease. Microarray analysis of 83 synovial samples provides insight into the expression-level differences between patients at the site of disease activity. Synovial samples from Rheumatoid Arthritis patients were obtained during joint resection and profiled using microarrays.

2014-04-22 | E-GEOD-48780 | biostudies-arrayexpress

RANK+TLR2+ Myeloid Subpopulation Converts Autoimmune to Joint Destruction in Rheumatoid Arthritis

Project description:Joint destruction is the major clinic burden in patients with rheumatoid arthritis (RA). It is unclear, though, how this autoimmune disease progresses to the point of deterioration of the joint. Here, we report that in a mouse model of RA the upregulation of TLR2 expression and its a(2,3) sialylation in RANK+ myeloid monocytes mediate the transition from autoimmunity to osteoclast fusion and bone resorption, resulting in joint destruction. The expression of a(2,3) sialyltransferases were significantly increased in RANK+TLR2+ myeloid monocytes, and their inhibition or treatment with a TLR2 inhibitor blocked osteoclast fusion. Notably, analysis of our single-cell RNA-sequencing (scRNA-seq) libraries generated from RA mice revealed a novel RANK+TLR2- subset that negatively regulated osteoclast fusion. Importantly, the RANK+TLR2+ subset was significantly diminished with the treatments. Moreover, the RANK+TLR2- subset could differentiate into a TRAP+ osteoclast lineage, but the resulting cells did not fuse to form osteoclasts. Our scRNA-seq data showed that Maf is highly expressed in the RANK+TLR2- subset, and the a(2,3) sialyltransferase inhibitor induced Maf expression in the RANK+TLR2+ subset. The identification of a RANK+TLR2- subset provides a potential explanation for TRAP+ mononuclear cells in bone and their anabolic activity. Further, TLR2 expression and its a(2,3) sialylation in the RANK+ myeloid monocytes could be effective targets to prevent autoimmune-mediated joint destruction.

2023-05-24 | GSE221704 | GEO

Comparison of Rheumatoid Arthritis Patient and Control Sample Serum Proteomes

Project description:Rheumatoid arthritis is an autoimmune inflammatory joint condition which primarily affects the synovium of joints, characterised by synovial inflammation as well as articular cartilage and underlying bone destruction. Within this study, the proteomes of serum obtained from rheumatoid arthritis patients, and appropriate human controls, were analysed using liquid chromatography-tandem mass spectrometry. ProteoMiner™ equalisation columns were used to deplete high abundant proteins and reduce the protein concentration dynamic range.

2022-04-04 | PXD020235 | Pride

RNA-seq of synovial biopsies from rheumatoid arthritis patients

Project description:Synovial biopsies from rheumatoid arthritis patients were obtained and profiled using RNA-seq. Patients were stratified according to the number of swollen joints they had (SJC, swollen joint count) and divided in three groups for the differential expression analysis: None (SJC = 0), Low (1<= SJC <= 8), High (SJC > 8).

2021-04-26 | E-MTAB-6684 | 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