Estrogen regulates stemness and senescence of bone marrow stromal cells to prevent osteoporosis via ERβ-SATB2 pathway.

摘要: Decline of pluripotency in bone marrow stromal cells (BMSCs) associated with estrogen deficiency leads to a formation defect osteoporosis. Special AT-rich sequence binding protein 2 (SATB2) is crucial for maintaining stemness and osteogenic differentiation BMSCs. However, whether SATB2 involved estrogen-deficiency associated-osteoporosis largely unknown. In this study, we found that mediated senescence BMSCs, primarily through receptor beta (ERβ). BMSCs from the OVX rats displayed increased weaker expression, stemness, differentiation, while could rescue these phenotypes. Inhibition ERβ or ERα confirmed was estrogen-mediated Furthermore, upregulation induction response elements (ERE) located at -488 gene. overexpression alleviated enhanced OVX-BMSCs. SATB2-modified transplantation prevent trabecular loss an ovariectomized rat model. Collectively, our study revealed role senescence, osteogenesis These results indicate prevents osteoporosis by promoting osteogenesis, inhibiting ERβ-SATB2 pathway. Therefore, novel anti-osteoporosis target