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Stimulation of RA SFBs with IL1 or PDGF-D

ABSTRACT: Synovial fibroblasts of 6 RA patients were treated with IL1 or PDGF-D. The aim of this study was to outline mechanism of the disease RA by a treatment with one of these cytokines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58203 | GEO | 2014/08/10

SECONDARY ACCESSION(S): PRJNA251647

REPOSITORIES: GEO

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Stimulation of RA SFBs with IL1 or PDGF-D

Project description:Synovial fibroblasts of 6 RA patients were treated with IL1 or PDGF-D. The aim of this study was to outline mechanism of the disease RA by a treatment with one of these cytokines. In total 6 patients were analyzed with 5 time points each (0h, 1h, 2h, 4h and 12h). The patients are biological replicates.

2014-08-10 | E-GEOD-58203 | biostudies-arrayexpress

The transcriptome analysis of regulatory networks in RA-FLSs

Project description:Rheumatoid arthritis (RA) is a common chronic inflammatory joint disease characterized by persistent synovial hyperplasia and progressive destruction of joint cartilage and bone.Fibroblast-like synoviocytes (FLSs), a prominent component of hyperplastic synovial pannus tissue, are the primary effector cells in RA synovial hyperplasia and invasion. However, the underlying molecular mechanisms remain unclear. Here, we apply transcriptome to assay the regulatory networks which contribute to the proliferation, migration and invasion of RA-FLSs .

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Homo sapiens

Project description:Stimulation of RA SFBs with IL1 or PDGF-D

| PRJNA251647 | ENA

TNFR2 is critical for TNF-induced rheumatoid arthritis fibroblast-like synoviocyte inflammation

Project description:Objectives: TNF-induced activation of fibroblast-like synoviocytes (FLS) is a critical determinant for synovial inflammation and joint destruction in rheumatoid arthritis (RA). The detrimental role of TNF-receptor 1 (TNFR1) has thoroughly been characterized. The contributions of TNFR2, however, are largely unknown. This study was performed to delineate the role of TNFR2 in human FLS activation. Methods: TNFR2 expression in synovial tissue samples was determined by immunohistochemistry. Expression of TNFR2 was silenced using RNAi or CRISPR/Cas9 technologies. Global transcriptional changes were determined by RNA-seq. QPCR, ELISA and immunoblotting were used to validate RNA-seq results and to uncover pathways operating downstream of TNFR2 in FLS. Results. TNFR2 expression was increased in RA when compared to OA synovial tissues. In particular, RA-FLS demonstrated higher levels of TNFR2 when compared to OA-FLS. TNFR2 expression in RA-FLS correlated with RA disease activity, synovial T- and B-cell infiltration. TNF and IL1 were identified as inflammatory mediators that upregulate TNFR2 in RA-FLS. Silencing of TNFR2 in RA-FLS markedly diminished the TNF-induced expression of inflammatory cytokines and chemokines, including CXCR3-binding chemokines and the B-cell activating factor TNFSF13B. Immunobiochemical analyses revealed that TNFR2-mediated expression of inflammatory mediators critically depends on STAT1. Conclusion: Our results define a critical role for TNFR2 in FLS-driven inflammation and unfold its participation in the unresolved course of synovial inflammation in RA.

2022-04-26 | GSE195557 | GEO

Tandem Mass Tag (TMT)-coupled LC-MS/MS in OA and RA patients synovial tissues

Project description:All the synovial tissue specimens for TMT relative quantitative proteomics and further experiments were obtained from the patients with RA or OA undergoing surgical joint replacement at the clinical of joint surgery (Xi'an Hong Hui Hospital, Xi'an Jiaotong University, China). The diagnosis of the patients were accorded to the criteria of the American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) in 2010.a quantitative proteomic profiling of synovial tissue obtained from RA and OA patients was carried out by using TMT labeling followed by high resolution mass spectrometry analysis. We have identified 4822 proteins out of which 510 proteins were found to be differentially expressed by ≥1.2 fold change in the synovial tissue from RA verses OA patients.

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by TL1A

Project description:TNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFκB by binding to its specific receptor death receptor 3 (DR3). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble TL1A in addition to Fas-ligand (FasL) and LIGHT and inhibits the signaling of TL1A via DR3. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNFα or IL-1β inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. Therefore, TL1A-DcR3/DR3 signaling may be involved in the pathogenesis of RA by modulating apoptosis and proliferation of RA-FLS. We hypothesized that TL1A regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by the ligation of TL1A.

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Project description:In the current study, we compared DNA methylation patterns using the Illumina 850k array technology between normal synovial fibroblasts and synovial fibroblasts from early (veRASF) and late stages of RA (estRASF) and transient, resolving arthritis (rSF). In doing so, we obtained a detailed view of changes in DNA methylation that occur during the development of RA from the earliest clinically apparent stages to established RA with its typical signs and symptoms.

2018-03-31 | E-MTAB-6582 | biostudies-arrayexpress

Illumina Humanmethylation450k array analysis in early synovial fibroblasts of RA patients before diagnosis

Project description:In the current study, we compared DNA methylation patterns using the Illumina 450k array technology between normal synovial fibroblasts and synovial fibroblasts from early (veRASF) and late stages of RA (estRASF) and transient, resolving arthritis (rSF). In doing so, we obtained a detailed view of changes in DNA methylation that occur during the development of RA from the earliest clinically apparent stages to established RA with its typical signs and symptoms.

2018-03-31 | E-MTAB-6581 | biostudies-arrayexpress

Human fibroblast stimulation with PDGF-BB or b-FGF

Project description:We analyzed gene expression in human fibroblasts stimulated by platelet-derived growth factor-BB (PDGF-BB) or basic fibroblast growth factor (bFGF) for 1h and 24h. The results of two independent experiments were merged. SAM analysis identified 116 relevant probe sets. Hierarchical clustering of these probe sets showed divergent early gene regulation by PDGF and FGF but overlapping late response. We first analyzed genes commonly regulated by PDGF-BB and b-FGF more than 2 fold after 24h of stimulation and we found that these two growth factors repressed FOXO. We then focused on the early gene expression response induced by both growth factors. We performed a fold change analysis and found 114 probe sets regulated by PDGF-BB and 42 probe sets regulated by b-FGF, 37 of which were shared between the two gene lists . Keywords: Time course, cell Treatment comparison

2009-03-16 | GSE14256 | GEO

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