ArticlePhysiological genomics2013
Analyses of synovial tissues from arthritic and protected congenic rat strains reveal a new core set of genes associated with disease severity.
Article in Physiological genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- DLX4 regulates rheumatoid arthritis fibroblast-like synoviocytes invasiveness and a cancer transcriptomic signature.Scientific reports · 2025Article
- Up-regulation of SELENBP1 in inflammatory macrophages promoted proliferation and migration of synovial fibroblasts by promoting ROS productionCentral-European journal of immunology · 2025Article
- Interleukin-17 contributes to Ross River virus-induced arthritis and myositis.PLoS pathogens · 2022Article
- A novel CD209 polymorphism is associated with rheumatoid arthritis patients in Taiwan.Journal of clinical laboratory analysis · 2021Article
- RTD-1 therapeutically normalizes synovial gene signatures in rat autoimmune arthritis and suppresses proinflammatory mediators in RA synovial fibroblasts.Physiological genomics · 2019Article
- Suppression and resolution of autoimmune arthritis by rhesus θ-defensin-1, an immunomodulatory macrocyclic peptide.PloS one · 2017Article
- Single-cell systems-level analysis of human Toll-like receptor activation defines a chemokine signature in patients with systemic lupus erythematosus.The Journal of allergy and clinical immunology · 2015Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Little is known about the genes regulating disease severity and joint damage in rheumatoid arthritis (RA). In the present study we analyzed the gene expression characteristics of synovial tissues from four different strains congenic for non-MHC loci that develop mild and nonerosive arthritis compared with severe and erosive DA rats. DA.F344(Cia3d), DA.F344(Cia5a), DA.ACI(Cia10), and DA.ACI(Cia25) rats developed mild arthritis compared with DA. We found 685 genes with significantly different expression between congenics and DA, independent of the specific congenic interval, suggesting that these genes represent a new nongenetic core group of mediators of arthritis severity. This core group includes genes not previously implicated or with unclear role in arthritis severity, such as Tnn, Clec4m, and Spond1 among others, increased in DA. The core genes also included Scd1, Selenbp1, and Slc7a10, increased in congenics. Genes implicated in nuclear receptor activity, xenobiotic and lipid metabolism were also increased in the congenics, correlating with protection. Several disease mediators were among the core genes reduced in congenics, including IL-6, IL-17, and Ccl2. Analyses of upstream regulators (genes, pathways, or chemicals) suggested reduced activation of Stat3 and TLR-related genes and chemicals in congenics. Additionally, cigarette smoking was among the upstream regulators activated in DA, while p53 was an upstream regulator activated in congenics. We observed congenic-specific differential expression and detection in each individual strain. In conclusion, this new nongenetically regulated core genes of disease severity or protection in arthritis should provide new insight into critical pathways and potential new environmental risk factor for arthritis.
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