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The effect of estrogen on bone requires ER alpha in nonhematopoietic cells but is enhanced by ER alpha in hematopoietic cells

Artikel i vetenskaplig tidskrift
Författare Petra Henning
Claes Ohlsson
Cecilia Engdahl
Helen H. Farman
Sara H Windahl
Hans Carlsten
Marie K Lagerquist
Publicerad i American Journal of Physiology-Endocrinology and Metabolism
Volym 307
Nummer/häfte 7
Sidor E589-E595
ISSN 0193-1849
Publiceringsår 2014
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Centre for Bone and Arthritis Research
Sidor E589-E595
Språk en
Länkar dx.doi.org/10.1152/ajpendo.00255.20...
Ämnesord estrogen, estrogen receptor-alpha, bone marrow transplantation, trabecular bone, cortical bone, RECEPTOR-ALPHA, FEMALE MICE, ADIPOSE-TISSUE, CORTICAL BONE, FAS LIGAND, MOUSE, OSTEOBLASTS, DEFICIENCY, ESTRADIOL, MEN, Endocrinology & Metabolism, Physiology
Ämneskategorier Fysiologi, Endokrinologi, Reumatologi och inflammation

Sammanfattning

The effects of estrogen on bone are mediated mainly via estrogen receptor (ER)alpha. ER alpha in osteoclasts (hematopoietic origin) is involved in the trabecular bone-sparing effects of estrogen, but conflicting data are reported on the role of ER alpha in osteoblast lineage cells (nonhematopoietic origin) for bone metabolism. Because Cre-mediated cell-specific gene inactivation used in previous studies might be confounded by nonspecific and/or incomplete cell-specific ER alpha deletion, we herein used an alternative approach to determine the relative importance of ER alpha in hematopoietic (HC) and nonhematopoietic cells (NHC) for bone mass. Chimeric mice with selective inactivation of ER alpha in HC or NHC were created by bone marrow transplantations of wild-type (WT) and ER alpha-knockout (ER alpha(-/-)) mice. Estradiol treatment increased both trabecular and cortical bone mass in ovariectomized WT/WT (defined as recipient/donor) and WT/ER alpha(-/-) mice but not in ER alpha(-/-)/WT or ER alpha(-/-)/ER alpha(-/-) mice. However, estradiol effects on both bone compartments were reduced (similar to 50%) in WT/ER alpha(-/-) mice compared with WT/WT mice. The effects of estradiol on fat mass and B lymphopoiesis required ER alpha specifically in NHC and HC, respectively. In conclusion, ER alpha in NHC is required for the effects of estrogen on both trabecular and cortical bone, but these effects are enhanced by ER alpha in HC.

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