Project description:To identify susceptibility genes concerning copy number variations (CNVs) in rheumatoid arthritis (RA), a case-control genome-wide CNV analyses was carried out by Roche Nimblegen array-based CGH. In this study, 15 RA patients and 1 control (Non-RA) were included.
Project description:Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease of unknown etiology and pronounced inter-patient heterogeneity. To characterize RA at the molecular level and to uncover key pathomechanisms, we performed whole-genome gene expression analyses. Synovial tissues from rheumatoid arthritis patients were compared to those from osteoarthritis patients and to normal donors. Keywords: disease state analysis
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.
Project description:Rheumatoid arthritis (RA) is a complex and clinically heterogeneous autoimmune disease. Microarray analysis of 83 synovial samples provides insight into the expression-level differences between patients at the site of disease activity. Synovial samples from Rheumatoid Arthritis patients were obtained during joint resection and profiled using microarrays.
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.
Project description:The transcriptome of PBMC from rheumatoid arthritis patient hasn't been compenhensively profiled, and heterogeneous characteristics of blood monocytes in RA patients are much unknown. We performed the single cell transcriptomic analysis of PBMC from rheumatoid arthritis (RA) patient, and monocyte populations were extracted during the analysis. CD127 expression associated expression pattern of inflammatory genes was identified in RA patient's blood monocytes.
Project description:Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic destructive arthritis. Although helper T cells are involved in the pathogenesis of RA, the characteristics of synovium-infiltrating CD4+ T cells are still largely unknown. In this study, we investigated synovium-infiltrating helper T cells of rheumatoid arthritis patients
Project description:miRNA differential expression in Rheumatoid arthritis(RA) blood: Microarray analysis of miRNAs in blood from RA and healthy donors.