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Endocrinology Vol. 142, No. 6 2205-2212
Copyright © 2001 by The Endocrine Society

ARTICLES

17ß-Estradiol Stimulates Expression of Osteoprotegerin by a Mouse Stromal Cell Line, ST-2, via Estrogen Receptor-{alpha}1

Mieko Saika, Daisuke Inoue, Shinsuke Kido and Toshio Matsumoto

First Department of Internal Medicine, University of Tokushima School of Medicine, Tokushima, Japan

Address all correspondence and requests for reprints to: Daisuke Inoue, M.D., First Department of Internal Medicine, University of Tokushima School of Medicine, 3–18-15 Kuramoto-cho, Tokushima 770-8503, Japan. E-mail: inoued{at}clin.med.tokushima-u.ac.jp

Osteoprotegerin (OPG) is a recently identified member of the tumor necrosis factor (TNF) receptor superfamily that regulates bone mass through an inhibitory action on osteoclast differentiation and function. To determine its potential roles of OPG in pathological changes in bone metabolism caused by estrogen deficiency, we investigated effects of estrogen on OPG expression by a mouse stromal cell line, ST-2, in vitro. Treatment of ST-2 cells with 17ß-E2 resulted in up-regulation of OPG expression at both the messenger RNA and protein levels. The effect was time and dose dependent and steroid specific. The stimulatory action of 17ß-E2 on OPG expression appeared to be mediated by the estrogen receptor-{alpha} (ER{alpha}) subtype because stable overexpression of ER{alpha}, but not of ERß, enhanced the OPG induction by 17ß-E2. Moreover, estrogen withdrawal after 5-day pretreatment, mimicking the event occurring in vivo at menopause, dramatically diminished the expression of OPG. These findings suggest that down-regulation of OPG after estrogen withdrawal contributes to the enhanced osteoclastic bone resorption and bone loss after menopause by enhancing RANK ligand-RANK system that lies downstream of a large number of bone-resorbing cytokines.




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