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Estrogen receptor-alpha in osteocytes is important for trabecular bone formation in male mice

Journal article
Authors Sara H Windahl
Anna E Börjesson
Helen H. Farman
Cecilia Engdahl
Sofia Movérare-Skrtic
Klara Sjögren
Marie Lagerquist
Jenny Kindblom
A. Koskela
J. Tuukkanen
P. D. Pajevic
J. Q. Feng
K. Dahlman-Wright
P. Antonson
J. A. Gustafsson
Claes Ohlsson
Published in Proceedings of the National Academy of Sciences of the United States of America
Volume 110
Issue 6
Pages 2294-2299
ISSN 0027-8424
Publication year 2013
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Centre for Bone and Arthritis Research
Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Pages 2294-2299
Language en
Links dx.doi.org/10.1073/pnas.1220811110
Keywords osteoblast-like cells, androgen receptor, knockout mice, fas ligand, older men, er-alpha, beta, deficient, estradiol, health, moto, Y.Omoto, YHumire, P.Humire, PGustafsson, J. -A.Gustafsson, JA2012424710BIOCHEMICAL AND
Subject categories Endocrinology

Abstract

The bone-sparing effect of estrogen in both males and females is primarily mediated via estrogen receptor-alpha (ER alpha), encoded by the Esr1 gene. ER alpha in osteoclasts is crucial for the trabecular bone-sparing effect of estrogen in females, but it is dispensable for trabecular bone in male mice and for cortical bone in both genders. We hypothesized that ER alpha in osteocytes is important for trabecular bone in male mice and for cortical bone in both males and females. Dmp1-Cre mice were crossed with ER alpha(flox/flox) mice to generate mice lacking ER alpha protein expression specifically in osteocytes (Dmp1-ER alpha(-/-)). Male Dmp1-ER alpha(-/-) mice displayed a substantial reduction in trabecular bone volume (-20%, P < 0.01) compared with controls. Dynamic histomorphometry revealed reduced bone formation rate (-45%, P < 0.01) but the number of osteoclasts per bone surface was unaffected in the male Dmp1-ER alpha(-/-) mice. The male Dmp1-ER alpha(-/-) mice had reduced expression of several osteoblast/osteocyte markers in bone, including Runx2, Sp7, and Dmp1 (P < 0.05). Gonadal intact Dmp1-ER alpha(-/-) female mice had no significant reduction in trabecular bone volume but ovariectomized Dmp1-ER alpha(-/-) female mice displayed an attenuated trabecular bone response to supraphysiological E2 treatment. Dmp1-ER alpha(-/-) mice of both genders had unaffected cortical bone. In conclusion, ER alpha in osteocytes regulates trabecular bone formation and thereby trabecular bone volume in male mice but it is dispensable for the trabecular bone in female mice and the cortical bone in both genders. We propose that the physiological trabecular bone-sparing effect of estrogen is mediated via ER alpha in osteocytes in males, but via ER alpha in osteoclasts in females.

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