Deficiency of β-arrestin 2 in mice-induced bone remodeling was associated with down-regulation of GPER1 expression

Abstract

Objective To determine the role of β-arrestin 2 on bone mineral density and microarchitecture, and its underlying mechanisms. Methods Ex vivo dual-energy-X-ray-absorptiometry(DXA) was used to measure the total body bone mineral density (BMD) and micro-CT scan was performed on mouse femora from female mice of wild type(WT) and β-arrestin 2 knockout(KO) at 16, 26, 30 weeks of age. RT-PCR was applied for the mRNA expression. Results Started from 16 weeks of age, total body BMD and the bone volume/total volume(BV/TV), trabecular number(Tb.N) in the femoral metaphysis of β-arrestin 2 KO female mice decreased dramatically. BMD decreased by 8.10%, 7.53%, 8.56%, BV/TV by 53.3%, 49.4%, 55.7% and Tb.N by 53.2%, 52.1%, 49.3% at 16, 26, 30 weeks of age, respectively, compared with those in WT mice(all P<0.05). In contrast, the trabecular pattern factor(Tb.Pf), trabecular separation(Tb.Sp), and structure model index(SMI) of the mice increased gradually with age, and reached statistically significant at age of 30 weeks(increased by 32.0%, 54.3%, and 23.7%, respectively, all P<0.05). RT-PCR showed that mRNA expression levels of osteoprotegrin, RANKL, and G protein-coupled estrogen receptor 1 in tibia from β-arrestin 2 KO mice were significantly lower than those in WT mice. Conclusion The effects of β-arrestin 2 on bone remodeling might be associated with G protein-coupled estrogen receptor1 signaling pathway. (Chin J Endocrinol Metab, 2015, 31: 897-901) Key words: β-Arrestin 2; Bone mineral density; Microarchitecture; Osteoprotegrin; G protein-coupled estrogen receptor 1