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      Minireview: Osteoprotective Action of Estrogens Is Mediated by Osteoclastic Estrogen Receptor-α

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          Abstract

          The osteoprotective action of estrogen in women has drawn considerable attention because estrogen deficiency-induced osteoporosis became one of the most widely spread diseases in developed countries. In men, the significance of estrogen action for bone health maintenance is also apparent from the osteoporotic phenotype seen in male patients with genetically impaired estrogen signaling. Severe bone loss and high bone turnover, including typical osteofeatures seen in postmenopausal women, can also be recapitulated in rodents after ovariectomy. However, the expected osteoporotic phenotype is not observed in female mice deficient in estrogen receptor (ER)-α or -β or both, even though the degenerative defects are clearly seen in other estrogen target tissues together with up-regulated levels of circulating testosterone. It has also been reported that estrogens may attenuate bone remodeling by cell autonomous suppressive effects on osteoblastogenesis and osteoclastogenesis. Hence, the effects of estrogens in bone appear to be complex, and the molecular role of bone estrogen receptors in osteoprotective estrogen action remains unclear. Instead, it has been proposed that estrogens indirectly control bone remodeling. For example, the enhanced production of cytokines under estrogen deficiency induces bone resorption through stimulation of osteoclastogenesis. However, the osteoporotic phenotype without systemic defects has been recapitulated in female (but not in male) mice by osteoclast-specific ablation of the ERα, proving that bone cells represent direct targets for estrogen action. An aberrant accumulation of mature osteoclasts in these female mutants indicates that in females, the inhibitory action of estrogens on bone resorption is mediated by the osteoclastic ERα through the shortened lifespan of osteoclasts.

          Abstract

          Estrogen is osteoprotective by attenuating bone resorption in females and males due to hormonally induced death of mature osteoclasts.

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          Author and article information

          Journal
          Mol Endocrinol
          Mol. Endocrinol
          mend
          Molecular Endocrinology
          Endocrine Society
          0888-8809
          1944-9917
          May 1, 2010
          : 24
          : 5
          : 877-885
          Affiliations
          Laboratory of Nuclear Signaling (Y.I., S.K., A.K., S.K.), Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan; College of Science and General Studies (A.K.), Alfaisal University, Riyadh 1153, Kingdom of Saudi Arabia; and ERATO (S.K.), Japan Science and Technology Agency, Saitama 332-0012, Japan
          Author notes
          Address all correspondence and requests for reprints to: Shigeaki Kato, Laboratory of Nuclear Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan. E-mail: uskato@ 123456mail.ecc.u-tokyo.ac.jp .
          Article
          PMC5417493 PMC5417493 5417493 4574
          10.1210/me.2009-0238
          5417493
          19910454
          13280aab-4535-4d7a-a24a-6460a6765526
          Copyright @ 2010
          History
          : 08 October 2009
          : 17 June 2009
          Categories
          Special Feature
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          877
          Minireview

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