Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275379 | ENA |
REPOSITORIES: ENA
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Project description:Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease involving primarily the synovial membranes and articular structures of multiple joints. A hallmark of RA is the pseudo-tumoral expansion of fibroblast-like synoviocytes (FLS), as these cells invade and finally destroy the joint structure. RA FLS have been therefore proposed as a therapeutic target. > TNF-related apoptosis-inducing ligand (TRAIL) has been described as a pro-apoptotic factor on malignant cells. The fact that fibroblasts-like-synoviocytes (FLS) in rheumatoid arthritis RA patients exhibit tumor like features led us to investigate the effect of TRAIL on ex-vivo RA FLS. We have previously described that TRAIL induces apoptosis only in a subset of RA FLS, but an induction of proliferation in the surviving cells. This observation corresponds to the pleiotropic effects of TRAIL observed on primary human tumor cells. We also observed that sensitivity to TRAIL-induced apoptosis varied in RA FLS from one patient to another, and was correlated with disease severity. We therefore screened for genes that were differentially expressed in RA FLS sensitive and resistant to TRAIL induced apoptosis in order to understand molecular factors making cells resistant or sensitive to TRAIL induced apoptosis.
2018-02-12 | GSE65908 | GEO
Project description:Fibroblast-like synoviocytes (FLS) are crucial in promoting articular inflammation and destruction in rheumatoid arthritis (RA). As the most abundant RNA modification, the function of m6A in RA FLS is still unclear. Here, we constructed FTO-knockdown FLS to explore the mechanism of FTO in regulating the aggressive behavior of RA FLS.
2024-12-31 | GSE241249 | GEO
Project description:Identify HIP1 binding proteins implicated in regulation of invasive property of Rheumatoid Arthritis (RA) fibroblast-like synoviocytes (FLS) by using FLS cell line from arthritic DA (highly invasive) and R6 (minimally invasive) arthritis-protected congenic rats, which differ in amino-acid changing HIP1 SNPs.
2024-04-18 | PXD051384 | Pride
Project description:To investigate the impact of mTOR inhibiton on TNFalpha-activated rheumatoid arthritis fibbroblast-like synoviocytes (RA-FLS)
2018-03-15 | E-MTAB-6457 | biostudies-arrayexpress
Project description:To address the regulation of interferon-stimulated genes expression by VGLL3 in fibroblast-like synoviocytes (FLS) of rheumatoid arthritis (RA) patients, VGLL3 was overexpressed in RA-FLS via a lentiviral vector. After four days of transfection, VGLL3-overexpressed RA-FLS and vector-transfected RA-FLS were subjected to RNA sequencing.
2022-08-17 | GSE200030 | GEO
Project description:Platelet microparticles (PMPs) are closely related to the activity of rheumatoid arthritis, and promote the migration and invasion of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs). In order to identify the possible mechanisms of the promotion effect on migration and invasion of RA-FLS by PMP, we used microarray analysis to detect the gene expressions of RA-FLSs after treatment with PMPs.
2017-06-06 | GSE99681 | GEO
Project description:Fibroblast-like synoviocytes (FLS) harbour active migration, invasion, proliferation and decreased cell-contact inhibition, and served as a crucial component in pathogenesis of rheumatoid arthritis. However, the mechanism underlying the aggressive behavior remain unclear. In this study, we established FTO-knockdown RA FLS to investigate the molecular mechanism.
2024-12-31 | GSE241253 | GEO
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:Activated fibroblast-like synoviocytes (FLS) are drivers of synovitis and structural joint damage in rheumatoid arthritis (RA). Despite the use of disease-modifying drugs, only about 50% of RA patients reach remission in real-world settings. We used an unbiased approach to investigate the effects of standard-of-care methotrexate (MTX) and a Janus kinase inhibitor, tofacitinib (TOFA), on gene expression in RA-FLS, in order to identify untargeted disease mediators.
2024-10-04 | GSE266310 | GEO
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.
2014-01-09 | GSE49604 | GEO