Gene expression of splenocytes in collagen-induced arthritis (CIA) model between Wildtype and Stinggt/gt mice.
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ABSTRACT:
PROVIDER: PRJNA597769 | ENA |
REPOSITORIES: ENA
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Project description:To explore the effect of sting molecule in CIA model, we decided to performed microarray for study at how the difference in gene expression profiles between wildtype and Stinggt/gt mice.
2019-12-27 | GSE142624 | GEO
Project description:The pathogenesis of rheumatoid arthritis (RA) is complicated and involves both innate and adaptive immunity [5]. The innate immunity such as macrophages or fibroblast-like synoviocytes (FLS) in the synovium can generate inflammatory mediators, including TNF-α, IL-1, IL-6, IL-17, IFN-γ, and chemo kines that lead to synovial inflammation, bone erosion, and cartilage damage [6-8]. The IL-17 signaling mediates the autoantibody production in collagen-induced arthritis (CIA) model [9]. However, the treatment response with an anti-IL17 monoclonal antibody in RA patients shows a high degree of heterogeneity [10]. The inhibitors of the Janus kinase (JAK) pathway are approved for RA patients [11]. These data suggest that the targeted multiple cytokines through the JAK pathway are useful for RA treatment. Disturbance of type I IFNs (IFNs-I) signaling and production drive autoimmune development [12]. The presymptomatic RA patients display an increase of IFNs-I before the onset of symptoms [13]. The RA patients also show the elevation of IFN- α in the synovial fluid and high expression of IFNs-I regulated gene in peripheral blood mononuclear cells (PBMC) [14]. However, the role of IFNs-I in arthritis and bone homeostasis has suggested the accelerating effect of arthritis and bone damage. The interferon-alpha receptor knockout mice develop arthritis severity higher than wild-type mice in the model of antigen-induced arthritis [15]. IFNs-I also affects the bone homeostasis by inhibiting osteoclastogenesis via receptor activator of nuclear factor-kappa B (RANK) pathway, and reduction of c-FOS expression [16-18]. Therefore, the goal of RA treatment with antagonizing the IFNs-I pathway has to be optimized between efficacy and potentially adverse effect. STING is a cytosolic DNA sensor that initiates the production of IFNs-I. STING functions have been reported as both pro-inflammatory signaling and negative regulator against inflammation [19-21]. The mutation in exon 5 of the STING gene results in gain function leading to initiate inflammation and cause the Sting associated vasculopathy with onset in infancy (SAVI) [22]. Loss of STING function rescues DNaseII-deficient mice from lethality and polyarthritis [23]. However, Sting-deficient lupus mice (MRL/Lpr mice) show higher and earlier mortality than Sting-sufficient MRL/Lpr mice [24]. The pathology also shows lymphoid hypertrophy with a higher amount of macrophages and granulocytes infiltration, autoantibodies, and cytokine [24]. The objective of this study was to identify the role of STING in the pathogenesis of rheumatoid arthritis using collagen-induced arthritis (CIA) model as a representative model of the human RA.
2020-06-26 | PXD018652 | Pride
Project description:The goal of this experiment is to profile longitudinal transcriptome changes during the development of murine arthritis in CIA mouse model. Male DBA1 mice (age between 10 to 12 weeks) were used in this study. CIA was induced by two immunizations with Type II collagen in Complete Freund’s adjuvant (CFA) at day 0, and with Type II collagen in Incomplete Freund’s adjuvant (IFA) at day 21. Bulk RNA-seq were done on right hind paws from control (non-immunized DBA1 mice) and CIA mice at different disease stages (up to 10 weeks after 1st immunization).
2022-03-24 | GSE193335 | GEO
Project description:Knee joint synovium was used for gene expression analysis of mouse collagen induced arthritis (CIA). Synovium was prepared at day 30 after initial sensitization from: healthy controls, CIA animals with no, with mild, with moderate, or with severe joint inflammation. Each sample group is represented by three replicates, each consisting of tissue collected from three to four animals. Keywords: disease severity analysis
2009-08-26 | GSE13071 | GEO
Project description:Knee joint synovium was used for gene expression analysis of mouse collagen induced arthritis (CIA). Synovium was prepared at day 30 after initial sensitization from: healthy controls, CIA animals with no, with mild, with moderate, or with severe joint inflammation. Each sample group is represented by three replicates, each consisting of tissue collected from three to four animals. Experiment Overall Design: The data set consists of 15 samples: five groups with three replicates each. One sample group is from healthy controls, the other groups are from CIA animals with different degress of joint inflammation.
2009-09-15 | E-GEOD-13071 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases, as well as their relevant mouse models such as CIA. We isolated joint samples pooled from six CIA mice or from six naM-CM-/ve control mice. Total RNA was extracted for the TaqManM-BM-. Low Density Assay v3.0
2012-12-19 | E-GEOD-37422 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases, as well as their relevant mouse models such as CIA.
2012-12-19 | GSE37422 | GEO
Project description:Fibroblast-like synoviocytes (FLS) were isolated from the inflamed joints of mice with collagen-induced arthritis (CIA) or the joints of naive littermates to characterise gene expression changes in response to chronic inflammation. Cells were isolated at two times of day (zeitgeber time, ZT4 and ZT16) to characterise diurnal variation in inflammatory symptoms and responses. FLS cells were isolated from joint digests based on Podoplanin expression prior to RNA extraction and library preparation for sequencing.
2024-06-06 | E-MTAB-13317 | biostudies-arrayexpress
Project description:The aim of the project is to analyze the plasma proteomic profile of an animal model of arthritis (Collagen Induced Arthritis; CIA) in response to different treatments. For this, plasma samples from mice under five different treatments were analyzed (N=6 per group): Vehicle, CIA, CIA + Δ9-THCA-A (20 mg / kg), CIA + Δ9-THCA-A (20 mg / kg) + T0070907 (5 mg / kg) and CIA + Δ9-THCA-A (20 mg / kg) + SR141716A (5 mg / kg).
2020-09-18 | PXD015274 | Pride
Project description:The molecular basis to autoimmune arthritis is unclear. Collagen Induced Arthritis (CIA) in mice, is a model that has many features that resemble Rheumatoid Arthritis (RA), although it does not perfectly duplicate RA. The study of CIA has provided insight into relevant pathogenesis and has aided in the identification of potential therapeutic targets. In this study we used Mouse Cytokine Expression Arrays to examine gene expression levels in joints at early, peak and decline stages during disease in DBA/1 mice. The aim of the study was to identify candidate molecules that may be involved in the development and progression of collagen-induced arthritis (CIA). Keywords: Disease State Analysis
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