E-MTAB-7798
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-7798 | ExpressionAtlas | 2023-06-16
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-7798-analysis-methods.tsv | Tabular | |||
| E-MTAB-7798-analytics.tsv | Tabular | |||
| E-MTAB-7798-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-7798-configuration.xml | Xml | |||
| E-MTAB-7798-g2_g1-mvaPlot.png | Other |
Items per page: 5 1 - 5 of 23 |
Similar Datasets
Project description:Pro-inflammatory cytokines drive functional deregulation of potassium channels in primary synovial fibroblasts
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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:Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells that plays critical roles in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) by using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. We analyzed the gene expression profiles of synovial fibroblasts that were treated with or without IL-17A. IL-17 induced gene expression in synovial fibroblasts from human temporomandibular joint was measured at 4 hours after treated with IL-17A (10 ng/ml) and untreated control samples. This experiment used one donor sample.
2015-11-05 | E-GEOD-74668 | 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.
2012-04-24 | GSE37520 | GEO
Project description:Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells that plays critical roles in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) by using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. We analyzed the gene expression profiles of synovial fibroblasts that were treated with or without IL-17A.
2015-11-05 | GSE74668 | GEO
Project description:Synovial fibroblasts (SF) are the main mesenchymal cell type constitutive in human synovial tissue. SF contribute to the homeostasis of normal joints by synthesizing extracellular matrix components and secreting the specific components of synovial fluid. SF are essential players in RA pathophysiology, they are the primary source of IL6 in the RA synovium contributing to perpetuate the inflammation in the joint. We used microarrays analysis to characterize the effector pro-inflammatory response of SF to TNFα and IL6/sIL6R signaling.
2021-06-01 | GSE132830 | GEO
Project description:The aim of this study was to characterize the surfaceome of primary equine chondrocytes isolated from healthy joints following exposure to the pro-inflammatory cytokines interleukin-1-beta (IL-1β) and tumour necrosis factor-alpha (TNF-α). We employed combined methodology that we recently developed for investigating the surfaceome in stem cells. Membrane proteins were isolated using an aminooxy-biotinylation technique and analysed by mass spectrometry using high throughput shotgun proteomics. Amongst the 431 unique cell surface proteins identified, a high percentage of low-abundance proteins, such as ion channels, receptors and transporter molecules were detected. A high number of proteins exhibited different levels of expression following chondrocyte stimulation with pro-inflammatory cytokines. LPR-1, thrombospondin, VDAC1-2 and annexin A1 were chosen for further analysis and validation by western blotting as proteins of special interest. Our results provide, for the first time, a repository for proteomic data on differentially expressed low-abundance membrane proteins on the surface of chondrocytes in response to pro-inflammatory stimuli.
2020-07-02 | PXD014773 | Pride
Project description:Synovial fibroblasts 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 tissue-destructive fibroblast phenotype in arthritis, we performed bulk RNA-sequencing analysis on the synovial fibroblasts which were isolated from Col6a1-Cre-Ets1-flox/flox (Ets1ΔFib) and Ets1-flox/flox (Ets1flox) mice.
2022-07-06 | GSE201310 | GEO
Project description:Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.
2018-06-04 | E-MTAB-6476 | ExpressionAtlas
Project description:The synovium secretes synovial fluid but is also richly innervated with nociceptors and acts as a gateway between avascular joint tissues and the circulatory system. Resident fibroblast-like synoviocytes’ (FLS) calcium-activated potassium channels (KCa) change in activity in arthritis models and this correlates with FLS activation. To deepen our understanding of the synovium in the context of synovial joint health and disease, the electrophysiological profile of FLS cells needs to be characterised, along with the ion channels that are present. Ion channels are an essential component of any cell membrane that controls ion movement in and out of the cell and play an important role in a multitude of cell regulating processes, typically by modulating the membrane potential To this end, we chose to perform an UNBIASED screen to identify/screen the ion channels that are transcribed in these cells and determine if this "channelome" changes with cytokine exposure. PCR/Westerns naturally bias toward the known proteins and transcripts and so we used Next Generation sequencing to scan the entire transcriptome. Objective: To determine the mechanism of this activation in an in vitro model of inflammatory arthritis; 72hr treatment with the cytokines TNFa and IL1b.
2020-03-06 | E-MTAB-7798 | biostudies-arrayexpress