Pharmacological Estrogen Administration Causes a FSH-Independent Osteo-Anabolic Effect Requiring ER Alpha in Osteoblasts

摘要: Postmenopausal osteoporosis is characterized by declining estrogen levels, and replacement therapy has been proven beneficial for preventing bone loss in affected women. While the physiological functions of bone, primarily inhibition resorption, have studied extensively, effects pharmacological administration are still poorly characterized. Since elevated levels follicle-stimulating hormone (FSH) suggested to be involved postmenopausal loss, we investigated whether skeletal response mediated a FSH-dependent manner. Therefore, treated wildtype FSHβ-deficicent (Fshb−/−) mice with 4 weeks subsequently analyzed their phenotype. Here observed that treatment resulted significant increase trabecular cortical mass both, Fshb−/− mice. Unexpectedly, this FSH-independent effect was not caused influencing but increasing formation. To understand cellular molecular nature osteo-anabolic next administered mouse models carrying cell specific mutant alleles receptor alpha (ERα). found ERα inactivation osteoclasts, while it blunted lacking osteoblasts or incapable DNA binding. Taken together, our findings reveal previously unknown administration, which independent FSH requires DNA-binding osteoblasts.