Department of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
J Endocrinol Invest. 2013 Jan;36(1):21-7. doi: 10.3275/8301. Epub 2012 Mar 22.
Although G-protein-coupled receptor, GPR30, has been considered as a G-protein-coupled estrogen receptor, conflicting results have been reported and the function of GPR30 in bone remains unresolved. The aim of this study was to clarify the functional role of GPR30 in osteoblasts using its derived cell line.
Immunohistochemical study revealed that GPR30 is expressed in human osteoblasts. Human fetal osteoblast cell lines, hFOB cells, which express GPR30 but lack estrogen receptor, were used for the in vitro experiments. Estradiol or raloxifene induced the proliferation of hFOB cells, which was accompanied by the activation of mitogen-activated protein (MAP) kinase. Those proliferative effects were completely abrogated by the transfection of GPR30 small interfering RNA, while the transfection alone did not affect the cell viability.
GPR30 is required for the proliferation of hFOB cells induced by estradiol or raloxifene. This proliferative effect was at least partly mediated via MAP kinase activation. These findings revealed a novel function of GPR30 in osteoblasts and might lead to a better understanding of how estrogen and selective estrogen receptor modulators show their osteoprotective effects.
尽管 G 蛋白偶联受体 GPR30 被认为是 G 蛋白偶联雌激素受体，但已有报道存在相互矛盾的结果，其在骨骼中的功能仍未得到解决。本研究旨在使用其衍生细胞系阐明 GPR30 在成骨细胞中的功能作用。
免疫组织化学研究显示 GPR30 表达于人类成骨细胞中。人胎成骨细胞系 hFOB 细胞表达 GPR30 但缺乏雌激素受体，用于体外实验。雌二醇或雷洛昔芬诱导 hFOB 细胞增殖，伴随着丝裂原激活蛋白（MAP）激酶的激活。用 GPR30 小干扰 RNA 转染完全阻断了这些增殖作用，而单独转染不会影响细胞活力。
GPR30 是雌二醇或雷洛昔芬诱导 hFOB 细胞增殖所必需的。这种增殖作用至少部分是通过 MAP 激酶激活介导的。这些发现揭示了 GPR30 在成骨细胞中的新功能，可能有助于更好地理解雌激素和选择性雌激素受体调节剂如何发挥其护骨作用。
