Histone deacetylases in RA: Epigenetics and epiphenomena

Aleksander M. Grabiec, Kris A. Reedquist

    Research output: Contribution to journalArticlepeer-review


    Reduced synovial expression of histone deacetylases (HDACs) is proposed to contribute to pathology in rheumatoid arthritis (RA) by enhancing histone-dependent access of transcription factors to promoters of inflammatory genes. In the previous issue of Arthritis Research & Therapy, Kawabata and colleagues provided independent evidence that HDAC activity is increased in the synovium and fibroblast-like synoviocytes (FLSs) of patients with RA and is paralleled by increased HDAC1 expression and synovial tumor necrosis factor-alpha (TNFα) production. Remarkably, stimulation of RA FLSs with TNFα specifically increases HDAC activity and HDAC1 expression, suggesting that changes in synovial HDAC activity and expression may be secondary to local inflammatory status. © 2010 BioMed Central Ltd.
    Original languageEnglish
    Article number142
    JournalArthritis Research and Therapy
    Issue number5
    Publication statusPublished - 11 Oct 2010


    • Arthritis
    • Enzymologic
    • Epigenesis
    • Gene Expression
    • Gene Expression Regulation
    • Genetic
    • Histone Deacetylases
    • Histone Deacetylases: metabolism
    • Humans
    • Rheumatoid
    • Rheumatoid: enzymology
    • Rheumatoid: immunology
    • Rheumatoid: pathology
    • Tumor Necrosis Factor-alpha
    • Tumor Necrosis Factor-alpha: biosynthesis


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