Journal
RHEUMATOLOGY
Volume 47, Issue 12, Pages 1785-1791Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ken368
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Funding
- The Arthritis Society of Canada [TAS 04/0031]
- Canadian Institutes of Health Research (CIHR) [IMHA-67519, MOP-88104]
- Canadian Arthritis Network
- Association Jacques Cartier
- Association pour la Recherche sur la Polyarthrite (ARP, France)
- The Arthritis Society of Canada
- CNRS
- Institute of Gender and Health (CIHR)
- Calgary Foundation-Grace Glaum Professor in Arthritis Research
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Objectives. Subchondral bone loss is a characteristic feature of inflammatory arthritis. Recently, estrogen receptor-related receptor- (ERR-), an orphan nuclear receptor, has been found to be involved in activation of macrophages. We hypothesized that ERR- 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 Freunds complete adjuvant. RNA was isolated from the bone and joints and expression of ERR- 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- is dysregulated in bones and joints in a mouse model of inflammatory arthritis. Specifically, we show that ERR- 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- 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- expression may precede and contribute to the destruction of cartilage and bone accompanying inflammatory arthritis.
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