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J. Biol. Chem., Vol. 275, Issue 28, 21372-21379, July 14, 2000

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Impaired Estrogen Sensitivity in Bone by Inhibiting Both Estrogen Receptor  and  Pathways^*

Sumito Ogawa^§, Masayo Fujita^§, Yasunori Ishii, Hiroshi Tsurukami^¶, Masami Hirabayashi, Kazuhiro Ikeda, Akira Orimo, Takayuki Hosoi^§, Masatsugu Ueda, Toshitaka Nakamura^¶, Yasuyoshi Ouchi^§, Masami Muramatsu, and Satoshi Inoue^§**

From the  Department of Biochemistry, Saitama Medical School, 38 Morohongo, Moroyama-machi, Iruma-gun, Saitama 350-0495, the ^§ Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, the ^¶ Department of Orthopaedic Surgery, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan, the  YS New Technology Institute, Inc., 519 Shimo-ishibashi, Ishibashi-machi, Simotsuga-gun, Tochigi 329-0512, Japan, and ^** CREST, Japan Science and Technology Corporation

Although it is well established that estrogen deficiency causes osteoporosis among the postmenopausal women, the involvement of estrogen receptor (ER) in its pathogenesis still remains uncertain. In the present study, we have generated rats harboring a dominant negative ER, which inhibits the actions of not only ER but also recently identified ER. Contrary to our expectation, the bone mineral density (BMD) of the resulting transgenic female rats was maintained at the same level with that of the wild-type littermates when sham-operated. In addition, ovariectomy-induced bone loss was observed almost equally in both groups. Strikingly, however, the BMD of the transgenic female rats, after ovariectomized, remained decreased even if 17-estradiol (E₂) was administrated, whereas, in contrast, the decrease of littermate BMD was completely prevented by E₂. Moreover, bone histomorphometrical analysis of ovariectomized transgenic rats revealed that the higher rates of bone turnover still remained after treatment with E₂. These results demonstrate that the prevention from the ovariectomy-induced bone loss by estrogen is mediated by ER pathways and that the maintenance of BMD before ovariectomy might be compensated by other mechanisms distinct from ER and ER pathways.

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