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Endocrinology Vol. 143, No. 9 3658-3670
Copyright © 2002 by The Endocrine Society

ARTICLE

Estrogen Receptor-Related Receptor {alpha} Impinges on the Estrogen Axis in Bone: Potential Function in Osteoporosis

Edith Bonnelye, Vanessa Kung, Catherine Laplace, Deborah L. Galson and Jane E. Aubin

Department of Anatomy and Cell Biology (E.B., V.K., J.E.A.), University of Toronto, Toronto, Ontario M5S 1A8, Canada; and The New England Baptist Bone and Joint Institute (C.L., D.L.G.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Dr. Jane E. Aubin, Department of Anatomy and Cell Biology, Faculty of Medicine, University of Toronto, Room 6255, Medical Sciences Building, 1 King’s College Circle, Toronto, Ontario M5S 1A8, Canada. E-mail: jane.aubin{at}utoronto.ca.

The orphan nuclear estrogen receptor-related receptor {alpha} (ERR{alpha}) is expressed by osteoblastic cells and plays a functional role in osteoprogenitor proliferation and differentiation. To dissect further the role of ERR{alpha} in bone, we investigated the effects of estrogen (E2) on ERR{alpha} both in vitro and in vivo. Chronic treatment of fetal rat calvaria cells with E2-stimulated bone nodule formation and up-regulated ERR{alpha} mRNA expression at early (10 h and d 8) but not later times in culture, suggesting a link between ERR{alpha} and E2 during osteoprogenitor proliferation. ERR{alpha} mRNA levels were significantly lower in ovariectomized adult rat bones vs. those of sham-operated rats early (1 d and 1 wk) post surgery, but levels returned to control levels thereafter. ERR{alpha} is also expressed in osteoclasts (tartrate-resistant acid phosphatase + multinucleated cells) in vivo and in vitro (RAW 264.7 cells) and ovariectomization lowered the OPG/receptor activator of nuclear factor {kappa}B ligand expression ratio. Down-regulation of ERR{alpha} expression via antisense treatment of rat calvaria cells not only inhibited osteogenesis but also increased adipocyte colony formation and changed the OPG/receptor activator of nuclear factor {kappa}B ligand ratio. These data suggest that ERR{alpha} is regulated by estrogen in bone in which it may play a functional role at several levels (osteoblasts, adipocytes, and osteoclasts) in E2 deficiency diseases such as osteoporosis.




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