Gene expression in rheumatoid arthritis synovial macrophages
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE10500 | GEO | 2008/02/14
SECONDARY ACCESSION(S): PRJNA107955
REPOSITORIES: GEO
Similar Datasets
Project description:Macrophages from RA synovial fluids were compared to primary human monocyte-derived macrophages.
2017-08-10 | GSE97779 | GEO
Project description:Macrophages from RA synovial fluids were compared to primary human blood-derived macrophages. Experiment Overall Design: Macrophages from synovial fluids of five RA patients were isolated by ficoll density gradient centrifugation, followed by positive selection of CD14+ cells using magnetic beads. The patientsâ?? diagnoses were determined by their physicians, in each case a Board-certified rheumatologist at the Hospital for Special Surgery, and were definite RA according to American College of Rheumatology criteria. De-identified samples were processed in an anonymous manner using a protocol approved by the Institutional Review Board of the Hospital for Special Surgery. Experiment Overall Design: Human peripheral blood mononuclear cells were isolated from venous blood of independent healthy donors by centrifugation on a Ficoll density gradient. Monocytes were obtained from PBMCs using anti-CD14 magnetic beads, and were >96% pure as verified by flow cytometry. Monocytes were differentiated into macrophages by culturing in RPMI 1640 medium supplemented with 10% fetal bovine serum and M-CSF (20 ng/ml). The viability and purity of macrophages was comparable in all conditions Experiment Overall Design: Gene expression was analyzed using Affymetrix microarrays and protocols.
2008-04-07 | E-GEOD-10500 | biostudies-arrayexpress
Project description:Treatment refractory Rheumatoid Arthritis (RA) is a major clinical challenge. Drug-free remission is uncommon but provides proof-of-concept that articular immune-homeostasis can be reinstated. In this project, we used single-cell RNA- to study the role of synovial tissue macrophages in maintaining disease remission. We have sequenced synovial tissue macrophages from individuals with healthy synovium (as evaluated by MRI), patients with undifferentiated arthritis (UPA), RA patients naïve to treatment, RA patients resistant to treatment and RA patients in disease remission
2020-04-18 | E-MTAB-8322 | biostudies-arrayexpress
Project description:To investigate the transcriptional profiles of distinct macrophage subsets residing within the inflammed RA synovium. RNA sequencing was perfomed on FACS sorted CD206+CD163+ and CD206-CD163- synovial tissue macrophages from RA synovial tissue and fluid samples.
2024-09-10 | GSE246421 | 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. Keywords: cell type comparison, disease state analysis
2008-10-14 | GSE9329 | GEO
Project description:Mast cells are phenotypically and functionally highly heterogeneous, and their state is possibly controlled by their local microenvironment. Therefore, concrete analyses are needed to understand whether mast cells act as powerful motivators or dispensable bystanders in specific diseases. Here, we evaluated the correlation between synovial mast cells and rheumatoid arthritis (RA) disease severity, and the efficacy of therapeutic interventions against mast cells. We showed that degranulation of mast cells in inflammatory synovial tissues of RA patients was induced via MAS-related G protein-coupled receptor X2 (MRGPRX2), and the expression of MHC class II (MHC II) and costimulatory molecules on mast cells were upregulated. These unique signaling response led to mast cell activation and promoted T cell responses, resulting in the progression of RA. Collagen-induced arthritis mouse models treated with a combination of anti-IL-17A and cromolyn sodium, a mast cell membrane stabilizer, showed significantly reduced clinical severity and decreased bone erosion. The findings of the present study suggest that synovial microenvironment-influenced mast cells contribute to RA and may provide a novel mast cell-targeting therapy for RA.
2024-01-07 | PXD038584 | Pride
Project description:Rheumatoid synoviocytes, which consist of fibroblast-like synoviocytes (FLS) and synovial macrophages (SM), are crucial for the progression of rheumatoid arthritis (RA). Particularly, FLS of RA patients (RA-FLS) exhibit invasive characteristics reminiscent of cancer cells, destroying cartilage and bone, although it remains unresolved how RA-FLS exhibit invasive phenotype. RA-FLS and SM originate differently from mesenchymal and myeloid cells, respectively, but share many pathologic functions. However, the molecular signatures and biological networks representing the distinct and shared features of the two cell types are unknown. Presently, we performed global transcriptome profiling of FLS and SM obtained from RA and osteoarthritis patients. By comparing the transcriptomes, we identified distinct molecular signatures and cellular processes defining invasiveness of RA-FLS and pro-inflammatory properties of RA synovial macrophages (RA-SM), respectively. Interestingly, under interleukin1β-stimulated condition, RA-FLS newly acquired pro-inflammatory signature mimicking RA-SM without losing invasive properties. We next reconstructed a network model that delineates the shared, RA-FLS-dominant (invasive), and RA-SM-dominant (inflammatory) processes. From the network model, we selected 13 genes, including POSTN and TWIST1, as novel regulator candidates responsible for FLS invasiveness. Of note, POSTN and TWIST1 expressions were elevated in independent RA-FLS and were further instigated by interleukin1β. In vitro functional assays demonstrated the requirement of POSTN and TWIST1 for migration and invasion of RA-FLS stimulated with interleukin1β. Taken together, our systems approach to rheumatoid synovitis provides a basis for identifying novel regulators responsible for pathological features of RA-FLS and RA-SM, demonstrating how a certain type of cells acquires functional redundancy under chronic inflammatory conditions. To identify molecular signatures of FLS and MLS in RA joints, we isolated FLS from synovial tissues of RA and osteoarthritis (OA) patients, obtained synovial macrophages from synovial fluid of RA patients, and differentiated control macrophages from peripheral blood of healthy subjects. Also, we stimulated FLS with IL1β, and then analyzed gene expression profiles of both IL1β-stimulated RA-FLS and OA-FLS
2014-01-09 | E-GEOD-49604 | biostudies-arrayexpress
Project description:Analysis of the role of LXR on the transcriptional signature of monocyte-derived macrophages generated in the presence of tumor ascitic fluids or rheumatoid arthritis synovial fluids. Methods: Human Peripheral Blood Mononuclear Cells (PBMC) were isolated from buffy coats from donors over a Lymphoprep gradient according to standard procedures. Monocytes were purified from PBMC by magnetic cell sorting using anti-CD14 microbeads (>95% CD14+ cells). Monocytes from independent donors (0.5 x 106 cells/ml, >95% CD14+ cells) were treated with DMSO (vehicle), 1 micromolar GW3965 or 1 micromolar GSK2033 for 1 hour, and then cultured in RPMI 1640 10% FBS supplemented with either 50% Tumor-derived Ascitic Fluid (TAF) or 20% Synovial Fluid from patients with active Rheumatoid Arthritis (RASF), at 37°C in a humidified atmosphere with 5% CO2 and 21% O2. After 72 hours, cells were lysed and RNA isolated for transcriptional analysis.
2022-03-16 | GSE181313 | GEO
Project description:Objective: To study epigenetic patterns in T lymphocytes that accumulate in rheumatoid arthritis (RA) synovium, we characterized DNA methylation of CD3+ T cells in peripheral blood and synovial tissue in RA and osteoarthritis (OA) patients. Methods: Genomic DNA of CD3+ T cells was isolated from RA (n = 8) and OA (n = 5) patients from blood or synovium at the time of arthroplasty using antibodies and magnetic beads. Methylation was measured using Illumina Infinium MethylationEPIC Kit. Differentially methylated loci (DMLs) and genes (DMGs) were identified using Welch’s t-test. Principal component analysis (PCA), hierarchical clustering and pathway analysis were used to determine relationships among groups. Results: Comparing DNA methylation of CD3+ T cells between peripheral blood and synovial tissue within each disease, 4615 and 164 DMLs were identified in RA and OA samples respectively, resulting in 832 and 36 DMGs. PCA showed that methylation differences in T cells were greater based on location (blood vs. synovium) than based on disease (RA vs. OA). Differentially modified pathways were significantly enriched between RA blood and synovial T cells, especially in genes related to complement, integrin cell surface interactions and P53 pathway. The limited number of DMGs identified between OA blood and synovial T cells did not conform to biologic pathways. Conclusion: The patterns of DNA methylation in RA show location-specific differences related to immune pathways, while methylation differences in OA are limited. The RA joint-specific signatures could be due to selective accumulation of T cell populations or expansion of differentially marked adaptive immune cells. Understanding epigenetic patterns could provide clues to the types of T cells that accumulate in the RA joint and identify potential therapeutic targets.
2021-02-01 | GSE164468 | GEO
Project description:Rheumatoid arthritis (RA) is a chronic autoinflammatory disorder that affects small joints. Despite intense efforts, there isno definitive marker yet for early diagnosis RA and for monitoring the progression of this disease. We sought to catalog the proteins present in the synovial fluid of patients with rheumatoid arthritis. To identify lower abundance proteins, we undertook two approaches – we depleted the abundant proteins using a multiple affinity removal system (MARS14) column and we enriched glycoproteins using a lectin affinity column. The peptides were analyzed by LC-MS/MS on a high resolution Fourier transform mass spectrometer.
2016-06-13 | PXD000740 | Pride