Expression data from mouse arthritis tarsal joints
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE61140 | GEO | 2015/03/01
SECONDARY ACCESSION(S): PRJNA260341
REPOSITORIES: GEO
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Project description:Pathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model. Three tarsal joints were sampled per clinical phase from the following clinical phases: Duration of clinical arthritis 0-3 days, duration of clinical arthritis 1-2 weeks, duration of clinical arthritis 3-4 weeks and duration of clinical arthritis minimum 3 weeks and declining (Twelve joints in total). For the clinical phase M-bM-^@M-^\DeclineM-bM-^@M-^] the joints had had a clinical score of 3 for minimum 3 weeks, after which the clinical score had declined minimum 1 score when the joint was sampled. For all other joints, the clinical score was 3 at the sampling time. The twelve joints were compared to three joints from non-induced control animals. The joints were processed and analysed separately (unpooledM-BM- ). The joints were snap-frozen in liquid N2 and stored at -80M-KM-^ZC. RNA was extracted using the mirVanaTM miRNA isolation kit (Ambion, Denmark), amplified and labelled using the Pico amplification kit (Nugen, San Carlos, USA), according to the manufacturersM-BM-4 instructions, followed by hybridisation to Mouse Gene 1.0ST microarrays (Affymetrix, Santa Clara, USA). The quality of the RNA was evaluated using RNA integrity numbers (RIN) and only samples with values of minimum 8.4 were chosen for further analysis.
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Project description:Rheumatoid arthritis is an autoimmune disease in which joint inflammation lead to progressive cartilage and bone destruction. Matrix metalloproteinases (MMP) implicated in homeostasis of extracellular matrix (ECM) play a central role in cartilage degradation. The aim of this study was to investigate the role of MMP-8 (collagenase-2) suppression in the K/BxN serum-transfer arthritis model. Three male mice of each following groups: MMP-8 wild type and arthritic mice, MMP-8 wild type without arthritis (wild type control), MMP-8 KO and arthritic mice and MMP-8 KO without arthritis (KO control) were selected for RNA extraction, from ankle joints, and hybridation on Affymetrix microarrays. Male mice were used because they showed a trend to higher arthritis severity compared to female mice. In arthritic mice, ankle joints were taken 7 days after arthritis induction.
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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.
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Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease. CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+ CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.
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Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease. CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+ CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.
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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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Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease.CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.
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