Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA357921 | ENA |
REPOSITORIES: ENA
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Project description:Oxylipins play important roles in various biological processes and are considered as mediators of inflammation for a wide range of diseases such as rheumatoid arthritis (RA). The purpose of this research was to study differences in oxylipin levels between a widely used collagen-induced arthritis (CIA) mice model and healthy control (Ctrl) mice. DBA/1J male mice (age: 6-7 weeks) were selected and randomly divided into two groups, viz. a CIA- and a Ctrl group. The CIA mice were injected intraperitoneal (i.p.) with the joint cartilage component collagen type II (CII) and an adjuvant injection of lipopolysaccharide (LPS). Oxylipin metabolites were extracted from plasma for each individual sample using solid phase extraction (SPE) and were detected with high performance liquid chromatography/tandem mass spectrometry (HPLC-ESI-MS/MS), using dynamic multiple reaction monitoring (dMRM). Both univariate and multivariate statistical analysis was applied. The results in univariate student's t-test revealed 10 significantly up- or down-regulated oxylipins in CIA mice, which were supplemented by another 6 additional oxylipins, contributing to group clustering upon multivariate analysis. The dysregulation of these oxylipins revealed the presence of ROS-generated oxylipins and an increase of inflammation in CIA mice. The results also suggested that the Collagen-induced arthritis might associate with dysregulation of apoptosis, possibly inhibited by activated NF- κ B because of insufficient PPAR-γ ligands.
2015-11-04 | MTBLS243 | MetaboLights
Project description:Genome wide gene expression analysis BQ.Ncf1.m1J mutated and BQ wild type mice
| PRJNA193300 | ENA
Project description:transcriptome of clostridioides infection and collagen induced arthritis in mice
| PRJNA615786 | ENA
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: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
2007-09-18 | GSE8915 | GEO
Project description:This study identifies molecular changes in hematopoietic stem cells (HSC) isolated from mice with chronic autoimmune arthritis induced using the collagen-induced arthritis (CIA) model.
2019-05-01 | GSE129511 | GEO
Project description:miRNAs expression in joint of Collagen-induced arthritis (CIA)
| PRJNA159965 | ENA
Project description:Time course of collagen-induced arthritis in DBA/1J male mice, synchronized on day 28 with 10ug LPS
2009-11-16 | E-TABM-661 | biostudies-arrayexpress
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:Cl-amidine treatment reduces autoantibody response in collagen-induced arthritis
| PRJNA130785 | ENA