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: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.
Project description:The purpose of this study was (1) to identify novel genes involved in the pathogenesis of Rheumatoid Arthritis (RA) disease, which may provide additional targets for therapeutic intervention and (2) to examine the molecular mechanisms associated with the response to anti-TNF treatment. Microarray analysis of LPS-stimulated whole blood from RA patients pre and post anti-TNF treatment was conducted. This study identified 818 transcripts, differentially expressed in RA patients pre-treatment compared to non-RA control samples. While a number of these genes were associated with RA in previous studies, validating our data, a number of novel genes with possible functions in RA disease were also identified. The number of transcripts (1051) significantly altered post anti-TNF treatment indicates the impact of anti-TNF therapy on systemic gene expression. A number of these transcripts were confirmed to be altered in a larger patient group and may represent potential genetic markers of a patient’s clinical response to anti-TNF treatment. Keywords: Expression profiling in RA disease pre and post anti-TNF treatment
Project description:Rheumatoid arthritis (RA) is a common chronic inflammatory joint disease characterized by persistent synovial hyperplasia and progressive destruction of joint cartilage and bone.Fibroblast-like synoviocytes (FLSs), a prominent component of hyperplastic synovial pannus tissue, are the primary effector cells in RA synovial hyperplasia and invasion. However, the underlying molecular mechanisms remain unclear. Here, we apply transcriptome to assay the regulatory networks which contribute to the proliferation, migration and invasion of RA-FLSs .
Project description:Ectopic lymphoid structures (ELS) can develop in rheumatoid arthritis (RA) synovial tissue, but the precise pathways of B cell activation and selection are not well understood. Here, we identified a unique B cell population in the synovium characterized by co-expression of a family of orphan nuclear receptors, NR4A1 (also known as NUR77), NR4A2 (NURR1) and NR4A3 (NOR1), that is highly enriched at both early and late stages of RA. See doi:10.1101/2021.05.14.443150 for details.
Project description:Analysis of the regulatory architecture of gene expression variation in CD4+ T cells from patients with active RA. We have integrated gene expression with genotyping data in order to identify eQTLs that characterize the gene expression of CD4+ T cells in active RA. CD4+ T cell RNA was extracted from 26 patients with active RA. All samples were used to study the genetic regulatory mechanisms of CD4+ T cells in active Rheumatoid Arthritis.
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 Two disease conditions (rheumatoid arthritis and osteoarthritis) in comparison to normal donors were investigated. For the two disease groups samples derived from three individual patients and two pools of patients were hybridised.
