| First Author | Henning P | Year | 2014 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 307 |
| Issue | 7 | Pages | E589-95 |
| PubMed ID | 25117411 | Mgi Jnum | J:215572 |
| Mgi Id | MGI:5605636 | Doi | 10.1152/ajpendo.00255.2014 |
| Citation | Henning P, et al. (2014) The effect of estrogen on bone requires ERalpha in nonhematopoietic cells but is enhanced by ERalpha in hematopoietic cells. Am J Physiol Endocrinol Metab 307(7):E589-95 |
| abstractText | The effects of estrogen on bone are mediated mainly via estrogen receptor (ER)alpha. ERalpha in osteoclasts (hematopoietic origin) is involved in the trabecular bone-sparing effects of estrogen, but conflicting data are reported on the role of ERalpha 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 ERalpha deletion, we herein used an alternative approach to determine the relative importance of ERalpha in hematopoietic (HC) and nonhematopoietic cells (NHC) for bone mass. Chimeric mice with selective inactivation of ERalpha in HC or NHC were created by bone marrow transplantations of wild-type (WT) and ERalpha-knockout (ERalpha(-/-)) mice. Estradiol treatment increased both trabecular and cortical bone mass in ovariectomized WT/WT (defined as recipient/donor) and WT/ERalpha(-/-) mice but not in ERalpha(-/-)/WT or ERalpha(-/-)/ERalpha(-/-) mice. However, estradiol effects on both bone compartments were reduced ( approximately 50%) in WT/ERalpha(-/-) mice compared with WT/WT mice. The effects of estradiol on fat mass and B lymphopoiesis required ERalpha specifically in NHC and HC, respectively. In conclusion, ERalpha in NHC is required for the effects of estrogen on both trabecular and cortical bone, but these effects are enhanced by ERalpha in HC. |
