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 17β-E2 promotes bone formation and POSTN expression at the endosteal surface. In vitro, 17β-E2 upregulated POSTN expression in OVX-BMSCs. POSTN overexpression activated the Wnt/β-catenin signalling pathway and enhanced osteogenic differentiation of OVX-BMSCs. Furthermore, knockdown of Postn blocks the involvement of 17β-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 17β-E2 reduces osteoporosis and promotes osteogenesis through the POSTN-Wnt/β-catenin pathway. POSTN could, therefore, be a novel target gene for anti-osteoporosis therapies.
Highlights
Postmenopausal osteoporosis is a systemic skeletal disease characterised by reduced bone mass and deterioration of bone microstructure, resulting in increased bone fragility and susceptibility to fracture [1, 2]
Femoral cortical bone thickness (CtTh) was lower in the OVX group than in the sham group at 14 weeks of age (Figure 1(c)), and the 17β-E2-stimulated femoral BM increased over 2 weeks
We found that 17β-E2 significantly increased CtTh and bone volume/total volume (BV/TV) at 16 weeks
Summary
Postmenopausal osteoporosis is a systemic skeletal disease characterised by reduced bone mass and deterioration of bone microstructure, resulting in increased bone fragility and susceptibility to fracture [1, 2]. Postmenopausal osteoporosis is becoming a major global health problem [3, 4]. Oestrogen is a key hormone in bone remodelling and bone morphology maintenance [5]. Oestrogen deficiency reduces the osteogenic capacity of bone marrow stromal cells (BMSCs) and increases osteoclast formation, causing defects in bone formation and osteoporosis [6]. Previous studies [7] have shown the osteoprotective action of oestrogen by regulating bone formation. Bones are not the only target structures of oestrogen; long-term use of oestrogen increases the risk of breast tumours and cardiovascular diseases [8]
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