Synovial biopsies of osteoarthritis patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE82107 | GEO | 2016/06/02
SECONDARY ACCESSION(S): PRJNA324067
REPOSITORIES: GEO
Similar Datasets
Project description:Synovial biopsies were obtained from osteoarthritis (OA) synovium to find genes upregulated during OA. The genes upregulated during OA can be used to identify disease characteristic genes. 10 microarrays of end-stage OA synovial biopsies were compared to 7 microarrays of synovial biopsies from individuals without a joint disease. Genes with >1.2-fold upregulation and P<0.05 in OA VS HC were selected from the analysis.
2016-06-02 | E-GEOD-82107 | biostudies-arrayexpress
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.
2012-12-01 | E-GEOD-41038 | biostudies-arrayexpress
Project description:Synovial biopsies were obtained from rheumatoid arthritis (RA) synovium and from subjects without a joint disease to find gene upregulated during RA. The promoters of genes upregulated during RA compared to HC can be used to obtain disease-regulated gene therapy.
2016-01-27 | GSE77298 | GEO
Project description:Increased interleukin (IL)-17A has been identified in joints affected by osteoarthritis (OA), but it is unclear how IL-17A, and its family members IL-17AF and IL-17F, can contribute to human OA pathophysiology. Therefore, we aimed to evaluate the gene expression and signalling pathway activation effects of the different IL-17 family members in chondrocytes and fibroblasts derived from cartilage and synovium of patients with end-stage knee OA. Chondrocytes and synovial fibroblasts derived from end-stage OA patients were treated with IL-17A, IL-17AF, or IL-17F, and gene expression was assessed with bulk RNA-Seq. Hallmark pathway analysis showed that IL-17 cytokines regulated several OA pathophysiology-related pathways including immune-, angiogenesis-, and complement-pathways in both chondrocytes and synovial fibroblasts derived from end-stage OA patients. While overall IL-17A induced the strongest transcriptional response, followed by IL-17AF and IL-17F, not all genes followed this pattern. Disease-Gene Network analysis revealed that IL-17A-related changes in gene expression in these cells are associated with experimental arthritis, knee arthritis, and musculoskeletal disease gene-sets. In conclusion, the association of IL-17-induced transcriptional changes with arthritic gene-sets supports a role for IL-17A in OA pathophysiology.
2021-06-02 | GSE171952 | GEO
Project description:Osteoarthritis (OA) is a leading cause of disability globally. Despite an emerging role for synovial inflammation in OA pathogenesis, attempts to target inflammation therapeutically have had limited success. A better understanding of the cellular and molecular processes occurring in the OA synovium is needed to develop novel therapeutic strategies. Here, we contrasted mononuclear phagocytes and T cells in the synovial tissue of OA patients and inflammatory-arthritis (IA) patients. Compared to IA, OA synovial tissue contained fewer CD45+ leukocytes, consisting mostly of macrophages. Macrophages in OA synovial tissues displayed activated phenotypes shown by expression of proteins folate-receptor-2 and CD86. Macrophage phenotype, proliferation characteristics and transcriptome profile by RNA-sequencing distinguished two subtypes of patients within OA. One subgroup was more similar to IA - ‘inflammatory-like OA’ (iOA), and another non-inflammatory/mechanical, subgroup distinct from IA - ‘classical OA’ (cOA). Gene Ontology (GO) pathway analysis revealed that the iOA subgroup is characterised by a cell proliferation signature, whereas the cOA subgroup is defined by cartilage remodelling features. Furthermore, iOA synovial tissue contained higher proportions of macrophages, expressing higher levels of the proliferation marker Ki-67, as compared to cOA synovial tissue. The identification of these two distinct OA subtypes provides new insight into the heterogeneity of OA at the synovial tissue level, and suggests distinct cellular mechanisms in disease pathogenesis. Our findings could lead to the stratification of OA patients for suitable disease-modifying treatments, and the identification of novel therapeutic targets.
2019-10-24 | GSE123492 | GEO
Project description:The aim of this study was to compare the gene expression pattern of synovial cells from inflammatory (I) or normal/reactive (N/R) areas of a synovial membrane harvested from the same osteoarthritis (OA) patient. This study is the first to identify different expression pattern between two areas of the synovial membrane in the same patient. These differences concern several key pathways involved in OA pathogenesis (inflammation, cartilage metabolism, Wnt signaling and angiogenesis). This analysis also provides interesting information regarding new potent intermediates as potentiel targets for the future therapeutic. Synovial tissues were obtained from 12 knee OA patients at the time of total knee replacement. The inflammatory status of the synovial membrane was characterized according to macroscopic criteria and sorted as N/R and I. Biopsies were cultured separately for 7 days. Microarray gene expression profiling between N/R and I areas was performed.
2013-05-20 | E-GEOD-46750 | biostudies-arrayexpress
Project description:mRNA expression levels in synovial fibroblasts in 6 rheumatoid arthritis patients versus 6 osteoarthritis patients. Experiment Overall Design: Synovial tissue was obtained from open joint replacement surgery or Experiment Overall Design: arthroscopic synovectomy. Patients with RA or OA (n = 6 each for gene expression analysis and further patients for validation experiments) were classified according to the ACR criteria.
2009-04-28 | E-GEOD-7669 | biostudies-arrayexpress
Project description:The aim of this study was to compare the gene expression pattern of synovial cells from inflammatory (I) or normal/reactive (N/R) areas of a synovial membrane harvested from the same osteoarthritis (OA) patient. This study is the first to identify different expression pattern between two areas of the synovial membrane in the same patient. These differences concern several key pathways involved in OA pathogenesis (inflammation, cartilage metabolism, Wnt signaling and angiogenesis). This analysis also provides interesting information regarding new potent intermediates as potentiel targets for the future therapeutic.
2013-05-20 | GSE46750 | GEO
Project description:Synovium is acutely affected following joint trauma and contributes to post-traumatic osteoarthritis (PTOA) progression. Little is known about discrete cell types and molecular mechanisms in PTOA synovium. We aimed to describe synovial cell populations and their dynamics in PTOA. Single-cell RNA-seq profiling of synovium revealed fibroblasts (comprised of various functional subsets), macrophages, endothelial cells and pericytes to be the predominanent synovial cell types, along with rarer populations including T cells, Schwann cells and mast cells. Cell types undergo profound changes in abundance and gene expression following joint injury.
2022-08-25 | GSE211584 | GEO
Project description:To determine whether extracellular vesicles were also present in human disease, we isolated and evaluated extracellular vesicles from synovial fluid from normal and OA patients at relatively advanced ages (70 - 80 years). Here we report the altered expression of synovial fluid extracellular vesicles-derived miRNAs in osteoarthritis compared to normal patients with age-relate degeneration to investigate potential biomarkers for OA diagnosis. The OA donors had clinical evidence of OA based on pain that led to total joint arthroplasty.
2019-02-18 | GSE126677 | GEO