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Rheumatology Advance Access published online on October 16, 2008
Rheumatology, doi:10.1093/rheumatology/ken368
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Estrogen receptor-related receptor-{alpha} (ERR-{alpha}) is dysregulated in inflammatory arthritis

E. Bonnelye1, N. Laurin1, P. Jurdic2, D. A. Hart3 and J. E. Aubin1

1Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada 2Institut de Génomique Fonctionelle de Lyon, UMR 5242, CNRS/INRA/ENS/Université Lyon1, IFR 128 Lyon Biosciences, Ecole Normale Superieure, Lyon, France and 3Department of Surgery, McCaig Institute for Bone and Joint Health, Faculty of Medicine, University of Calgary, AB, Canada.

Correspondence to: J. E. Aubin, Department of Molecular Genetics, Faculty of Medicine, University of Toronto, Room 6233, Medical Sciences Building, 1 King's College Circle, Toronto, ON M5S 1A8, Canada. E-mail: jane.aubin{at}utoronto.ca


  Abstract

Objectives. Subchondral bone loss is a characteristic feature of inflammatory arthritis. Recently, estrogen receptor-related receptor-{alpha} (ERR-{alpha}), an orphan nuclear receptor, has been found to be involved in activation of macrophages. We hypothesized that ERR-{alpha} which is expressed and also functional in articular chondrocytes, osteoblasts and osteoclasts, may be involved in rodent models of inflammatory arthritis.

Methods. Erosive arthritis was induced in DBA/1 mice by injection of type II collagen in Freund's complete adjuvant. RNA was isolated from the bone and joints and expression of ERR-{alpha} and cartilage (GDF5 and Col2a1) and bone [bone sialoprotein (BSP) and osteocalcin (OCN)] markers was analysed by semi-quantitative PCR.

Results. We report for the first time that the expression of ERR-{alpha} is dysregulated in bones and joints in a mouse model of inflammatory arthritis. Specifically, we show that ERR-{alpha} expression is down-regulated early in bone and later in joints of mice with type II CIA. Concomitantly, temporal changes were observed in GDF-5 and Col2a1 expression in joints following both initial injection and booster injection of type II collagen. Similarly, down-regulation of ERR-{alpha} mRNA expression in subchondral bone in mice with induced joint inflammation was also paralleled by down-regulation of markers of bone formation (BSP, OCN).

Conclusions. These data suggest that dysregulation of ERR-{alpha} expression may precede and contribute to the destruction of cartilage and bone accompanying inflammatory arthritis.

KEY WORDS: Joint, Bone, Rheumatoid arthritis, Nuclear receptor, Estrogen receptor-related receptor

Present addresses: E. Bonnelye, INSERM UMR 664, Faculté de Médecine RTH Laennec, Rue Guillaume Paradin. 69372 Lyon Cedex 08, France; N. Laurin, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada.

Submitted 7 March 2008; revised version accepted 11 August 2008.
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