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Gene expression from fibroblast-like synoviocytes (FLS) of three patients with rheumatoid arthritis (RA) that were cultured in four conditions: control medium (Basal), ATRA, TNF and ATRA+TNF.

ABSTRACT: The aim of this study was to investigate the response of FLS from RA patients to retinoic acid and retinoic acid combined with the central cytokine of RA, TNF.

ORGANISM(S): Homo sapiens

PROVIDER: GSE120785 | GEO | 2019/12/09

REPOSITORIES: GEO

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Identification of genes regulating TRAIL-induced apoptosis in rheumatoid arthritis fibroblasts-like synoviocytes (RA FLS)

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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 NFM-NM-:B 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 TNFM-NM-1 or IL-1M-NM-2 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. RA-FLS were obtained from 4 RA patients (sample1-4). Each sample was incubated with either 1.0 M-NM-<g/ml recombinant human TL1A protein or phosphate buffered saline (PBS) diluted with serum-free Opti-MEM medium as non-stimulated control for 12 hours at 37M-BM-0C with 5% CO2. Gene expression in RA-FLS stimulated by TL1A was compared with that of their respective non-stimulated controls.

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

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by DcR3

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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 including rheumatoid arthritis (RA) 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. 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 TL1A.

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by DcR3

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

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Transcriptional responses to TNF following HFl treatment of primary rheumatoid arthritis fibroblast like synoviocytes (RA-FLS)

Project description:Transcriptional responses to TNF following HFl treatment of primary rheumatoid arthritis fibroblast like synoviocytes (RA-FLS)

| PRJNA606298 | ENA

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