ArticleArthritis and rheumatism2013
Differentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse models.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Computational Insights into the Polypharmacological Landscape of BCR-ABL Inhibitors: Emphasis on Imatinib and Nilotinib.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Tozasertib activates anti-tumor immunity through decreasing regulatory T cells in melanoma.Neoplasia (New York, N.Y.) · 2024Article
- Cyclopenta[ACS omega · 2020Article
- Clinical epigenetics and multidrug-resistant bacterial infections: host remodelling in critical illness.Epigenetics · 2020Review
- DNA Methylation-Governed Gene Expression in Autoimmune Arthritis.International journal of molecular sciences · 2019Review
- Trained Innate Immunity Not Always Amicable.International journal of molecular sciences · 2019Review
- DrugGenEx-Net: a novel computational platform for systems pharmacology and gene expression-based drug repurposing.BMC bioinformatics · 2016Article
- Aurora kinase a regulates m1 macrophage polarization and plays a role in experimental autoimmune encephalomyelitis.Inflammation · 2015Article
- Epigenetics in the pathogenesis of rheumatoid arthritis.BMC medicine · 2014Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveTo identify epigenetic factors that are implicated in the pathogenesis of rheumatoid arthritis (RA), and to explore the therapeutic potential of the targeted inhibition of these factors.
methodsPolymerase chain reaction (PCR) arrays were used to investigate the expression profile of genes that encode key epigenetic regulator enzymes. Mononuclear cells from RA patients and mice were monitored for gene expression changes, in association with arthritis development in murine models of RA. Selected genes were further characterized by quantitative reverse transcription-PCR, Western blot, and flow cytometry methods. The targeted inhibition of the up-regulated enzymes was studied in arthritic mice.
resultsA set of genes with arthritis-specific expression was identified by the PCR arrays. Aurora kinases A and B, both of which were highly expressed in arthritic mice and treatment-naive RA patients, were selected for detailed analysis. Elevated aurora kinase expression was accompanied by increased phosphorylation of histone H3, which promotes proliferation of T lymphocytes. Treatment with VX-680, a pan-aurora kinase inhibitor, promoted B cell apoptosis, provided significant protection against disease onset, and attenuated inflammatory reactions in arthritic mice.
conclusionArthritis development is accompanied by changes in expression of a number of epigenome-modifying enzymes. Drug-induced down-regulation of the aurora kinases, among other targets, seems to be sufficient to treat experimental arthritis. Development of new therapeutics that target aurora kinases can potentially improve RA management.
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