Endocrine Abstracts

Estrogen plays an important role on bone metabolism. However, the lacking of estrogen is proven a high risk to induce OP in post menopause women associated with bone metabolism problems. Furthermore, bone metabolism is strongly correlated with mechanical forces. It is proposed that mechanical forces, such as fluid shear stress and stretch, can modulate the function of bone cells. The OP patients’ bone seems lose this major function about functional adaptation and bone strength reduced. So, our study is to investigate whether estrogen affects the mechanical sensitivity of osteoblasts. First, we keep MG63 (osteoblasts-like cells) in estrogen-less condition. The applied shear stress (12 dyne/cm²) induces transient phosphorylations of extracellular signal-regulated kinase (ERK) and p38 which reaches peak at 30 min. It also induces transient expressions of cyclooxygenase-2 (Cox-2) and c-fos in 2 h. We pretreat estrogen 6 h ago and then apply shear stress for 30 and 60 min. The results reveal that estrogen enhances the expression of phosphoryaltion of ERK and p38. Meanwhile, estrogen enhances the gene expression including cox-2 and c-fos. According our results, it shows estrogen augments the shear stress -induced signaling and gene expression in MG63 cells. We also find treated estrogen 6 h can significantly increase expression of beta-1 integrins which act as mechanoreceptor. The phosphorylation of MAPK pathway and gene expression induced by flow or combining estrogen and flow are totally blocked by transfection of integrin beta-1 si-RNA. According our results, estrogen plays an important role in mechanical sensitivity of osteoblasts. Estrogen increases the number of mechanoreceptor, like integrin beta-1, and raises mechanical sensitivity of cell. It might explain why OP patients associate with bone mass losing and no functional adaptation of their bone.