Mus musculus
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ABSTRACT:
PROVIDER: PRJNA230637 | ENA |
REPOSITORIES: ENA
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Project description:To understand differences in the pathogenesis of synovial hyperplasia during TNF-induced arthritis, we compared the global gene expression of hTNFtg and hTNFtg;Rsk2-/y primary synovial fibroblasts.
2014-12-04 | GSE52992 | GEO
Project description:Rheumatoid arthritis (RA), a chronic and systemic disease of unknown etiology, is characterized by hyperplasia of synovial cells, which ultimately lead to the destruction of cartilage and bone. To elucidate the molecular mechanisms that lead to RA, we analyzed synovial cells established from patient with RA by oligonucleotide microarrays. Gene expression profiles reveal a novel pathophysiologic function of RA synovial cells as a generator of oxidative stress, and a self-defense mechanism against self-generated oxidative stress. Experiment Overall Design: We isolated synovial cell culture from patients with rheumatoid arthritis and osteoarthritis. Fibroblast from patient with osteoarthritis was used for the reference.
2008-10-26 | E-GEOD-9329 | biostudies-arrayexpress
Project description:To understand differences in the pathogenesis of synovial hyperplasia during TNF-induced arthritis, we compared the global gene expression of hTNFtg and hTNFtg;Rsk2-/y primary synovial fibroblasts. Murine fibroblast-like synoviocytes (FLS) were isolated from the hind paws of hTNFtg and hTNFtg;Rsk2-/y (background: C57BL/6) 6-9 week-old mice via collagenase digestion. The cells of two mice were pooled and cultivated for at least 3 passages before usage. For characterization, the cells were tested for the surface expression of CD90.2 and VCAM1 by flow cytometric analysis, whereas CD11b as a monocytic marker had to be absent. Total RNA was extracted using the RNeasy Mini kit (Qiagen). The integrity and amount of isolated RNA was assessed for each sample using an Agilent 2100 Bioanalyzer (Agilent, Waldbronn, Germany) and a NanoDrop ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE). Double-stranded complementary RNA was synthesized from 1 M-BM-5g total RNA using Message AmpII Biotin (Ambion, USA). Fifteen micrograms of fragmented cRNA of each sample were hybridized to six MG_U430_2 GeneChips (Affymetrix). Hybridization was performed in a Hybridization Oven 640, and chips were washed and stained in the Fluidics Station 450 (both Affymetrix). Finally, the arrays were scanned with a GeneChip Scanner 3000 using the GCOS software, version 1.4, both Affymetrix. All relevant GCOS data of quality checked microarrays were analyzed with High Performance Chip Data Analysis (HPCDA, unpublished), using the BioRetis database (www.bioretis-analysis.de), as described and validated previously.
2014-12-04 | E-GEOD-52992 | biostudies-arrayexpress
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 .
2020-01-08 | GSE128813 | GEO
Project description:Time-course gene expression profiles of the synovial tissues in collagen-induced arthritis
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Project description:To examine patterns of gene expression in ankle synovial fluid cells and peripheral blood leukocytes during serum transferred arthritis. A time-course microarray analysis of serum-transferred arthritis was performed, examining ankle tissue, synovial fluid, and peripheral blood leukocytes.
2011-02-24 | E-GEOD-27492 | biostudies-arrayexpress
Project description:Inflammatory arthritis is associated with bone loss and fractures due to abnormal bone remodelling. Bone remodelling is 'uncoupled' with bone resorption increased and bone formation suppressed. These changes resemble those seen in patients treated with therapeutic glucocorticoids, and in both of these situations, altered wnt signalling is implicated. Recent studies have highlighted the importance of the synovial fibroblast in mediating abnormal bone remodelling during inflammation. The wnt antagonist dickkopf-1 (DKK1) is secreted by synovial fibroblasts in response to inflammation, and this protein has been proposed to be a master regulator of bone remodelling in inflammatory arthritis. Here we show that DKK1 expression by primary human synovial fibroblasts is more potently regulated by glucocorticoids than pro-inflammatory cytokines. Glucocorticoids, but not TNF-alpha, regulated expression of multiple wnt agonists and antagonists in favour of inhibition of wnt signalling. In vitro TNF-alpha and IL1-beta indirectly regulate DKK1 production through increased expression of the glucocorticoid activating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). These results demonstrate that the links between synovial inflammation, altered wnt signalling and bone remodelling may not be direct but are dependent on local activation of endogenous glucocorticoids. Human fibroblast-like synoviocytes isolated from patients with rheumatoid arthritis treated with either vehicle, TNF or dexamethasone (dex). Gene arrays for control, TNF and dexamethasone treatments were performed on three separate synovial fibroblast cell lines isolated from three rheumatoid arthritis patients. All fold changes displayed are the combined results of the three separate fibroblast lines.
2012-04-24 | E-GEOD-37520 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:The destruction of bone and cartilage results in a loss of joint functionality, critically impairing the quality of life in arthritis patients. Synovial fibroblasts (SFs) critically contribute to the pathogenesis of rheumatoid arthritis (RA) by acquiring either a pro-inflammatory or tissue-destructive phenotype. To explore the molecular mechanisms underlying the pathogenic fibroblast phenotype in arthritis, we performed single-cell RNA sequencing (scRNA-seq) on the synovial cells which were isolated from collagen-induced arthritis (CIA) mice.
2022-07-06 | GSE192504 | GEO
Project description:Fibroblast-like synoviocytes (FLSs) are critical for synovial aggressiveness and joint destruction in rheumatoid arthritis (RA).The role and expression patterns of long noncoding RNAs (lncRNAs) in RA are largely unknown. We performed lncRNA and mRNA microarrays to identify differentially expressed lncRNAs and mRNAs in fibroblast-like synoviocytes from rheumatoid arthritis patients compared with fibroblast-like synoviocytes from trauma patients.
2018-09-07 | GSE103578 | GEO