Periostin Mediates Oestrogen-Induced Osteogenic Differentiation of Bone Marrow Stromal Cells in Ovariectomised Rats.

ABSTRACT

Osteoporosis is a metabolic disease that results in the progressive loss of bone mass, which, in postmenopausal women, is related to oestrogen deficiency. Periostin (POSTN) plays a key role in the early stages of bone formation. However, whether POSTN participates in oestradiol regulation of osteogenic differentiation of bone marrow stromal cells (BMSCs) from ovariectomised (OVX) rats remains unclear. In vivo, using microcomputed tomography (micro-CT), immunohistochemistry, and dynamic analysis of femurs, we found that 17ß-E2 promotes bone formation and POSTN expression at the endosteal surface. In vitro, 17ß-E2 upregulated POSTN expression in OVX-BMSCs. POSTN overexpression activated the Wnt/ß-catenin signalling pathway and enhanced osteogenic differentiation of OVX-BMSCs. Furthermore, knockdown of Postn blocks the involvement of 17ß-E2 in the osteogenic differentiation of OVX-BMSCs. Collectively, our study indicated the role of POSTN in the osteogenesis and stemness of OVX-BMSCs and proves that 17ß-E2 reduces osteoporosis and promotes osteogenesis through the POSTN-Wnt/ß-catenin pathway. POSTN could, therefore, be a novel target gene for anti-osteoporosis therapies.