Expression data from fibroblast-like synoviocytes (FLS) transfected with mimic-miR-23b or mimic-NC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE37427 | GEO | 2012/12/19
SECONDARY ACCESSION(S): PRJNA159963
REPOSITORIES: GEO
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Project description:We found microRNA miR-23b was down-regulated in local inflammatory tissues of autoimmune disease such as RA, SLE and related mouse models such as CIA, lpr, EAE. Re-expression of miR-23b significantly inhibits autoimmune pathogenesis of CIA, Lpr and EAE. To identify potential targets of miR-23b, we use microarray gene-expression analysis to identify transcripts which could be repressed by miR-23b. RA: rheumatoid arthritis, CIA: Collagen-induced arthritis, SLE: systemic lupus erythematosus, EAE: experimental autoimmune encephalomyelitis We tansfected fibroblast-like synoviocytes (FLS) with mimic-miR-23b or mimic-NC.Cells were collected and total RNA was extracted for the Affymetrix GeneChip® Human Genome U133 Plus 2.0 Array
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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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