Histone deacetylases in RA: Epigenetics and epiphenomena

Aleksander M. Grabiec; Kris A. Reedquist

doi:10.1186/ar3137

Histone deacetylases in RA: Epigenetics and epiphenomena

Aleksander M. Grabiec, Kris A. Reedquist

Research output: Contribution to journal › Article › peer-review

Abstract

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 language	English
Article number	142
Journal	Arthritis Research and Therapy
Volume	12
Issue number	5
DOIs	https://doi.org/10.1186/ar3137
Publication status	Published - 11 Oct 2010

Keywords

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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title = "Histone deacetylases in RA: Epigenetics and epiphenomena",

abstract = "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. {\textcopyright} 2010 BioMed Central Ltd.",

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AU - Reedquist, Kris A.

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N2 - 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.

AB - 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.

KW - Arthritis

KW - Enzymologic

KW - Epigenesis

KW - Gene Expression

KW - Gene Expression Regulation

KW - Genetic

KW - Histone Deacetylases

KW - Histone Deacetylases: metabolism

KW - Humans

KW - Rheumatoid

KW - Rheumatoid: enzymology

KW - Rheumatoid: immunology

KW - Rheumatoid: pathology

KW - Tumor Necrosis Factor-alpha

KW - Tumor Necrosis Factor-alpha: biosynthesis

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JO - Arthritis Research and Therapy

JF - Arthritis Research and Therapy

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M1 - 142

ER -

Histone deacetylases in RA: Epigenetics and epiphenomena

Abstract

Keywords

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