| First Author | Määttä JA | Year | 2013 |
| Journal | FASEB J | Volume | 27 |
| Issue | 2 | Pages | 478-88 |
| PubMed ID | 23073829 | Mgi Jnum | J:291914 |
| Mgi Id | MGI:6444976 | Doi | 10.1096/fj.12-213587 |
| Citation | Maatta JA, et al. (2013) Inactivation of estrogen receptor alpha in bone-forming cells induces bone loss in female mice. FASEB J 27(2):478-88 |
| abstractText | The role of the estrogen receptor alpha (ERalpha) in bone-forming cells is incompletely understood at present. To examine the in vivo effects of ERalpha in these cells, we generated a mouse strain in which the ERalpha gene is inactivated in osteoblasts via osteocalcin promoter-regulated cyclic recombinase (Cre) activity (ERalpha(DeltaOB/DeltaOB)). This enabled micro-computed tomography- and histomorphometry-based analysis of ERalpha-mediated effects in bone-forming cells in mice, in which the systemic ERalpha-mediated effects are intact. In female ERalpha(DeltaOB/DeltaOB) mice, trabecular and cortical bone volumes were significantly reduced (31.5 and 11.4%, respectively) at 3.5 mo of age compared with control ERalpha(fl/fl) animals, and their response to ovariectomy was small compared with that of controls. In contrast with females, no differences could be detected in the bone phenotype of young males, whereas in 6-mo-old ERalpha(DeltaOB/DeltaOB) males, trabecular bone volume (Tb.BV) was decreased (27.5%). The ERalpha inactivation-related effects were compared with those of controls having a similar genetic background. Parental osteocalcin-Cre mice did not show Cre-related changes. Our results suggest that in female mice, Tb.BV and cortical bone volume are critically dependent on the ERalpha regulation of osteoblasts, whereas in male mice, osteoblastic ERalpha is not required for the regulation of bone formation during rapid skeletal growth, but it is involved in the maintenance of Tb.BV. |
