The skeletal responsiveness to mechanical loading is enhanced in mice with a null mutation in estrogen receptor-beta.
The skeletal responsiveness to mechanical loading is enhanced in mice with a null mutation in estrogen receptor-beta.
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雌激素受体-β 无效突变的小鼠的骨骼对机械负荷的反应性增强。
DOI：
10.1152/ajpendo.00189.2007
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Turner,CH
中科院分区：
文献类型：
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作者：
Saxon,LK;Robling,AG;Castillo,AB;Mohan,S;Turner,CH
由体力活动引起的机械负荷可以刺激骨形成并加强骨骼。雌激素受体（ER）在施加机械负荷后在骨细胞中启动的信号级联中起一定作用。我们假设ER-β影响骨对机械负荷的反应性。为了验证我们的假设，16周龄的ER-β无效突变（ER-β−/−）的雄性和雌性小鼠的右前肢每天接受短时间的负荷。所使用的加载技术已被证明可以增加尺骨中的骨形成。每次加载回合包括连续3天每天施加30 s内的60次压缩载荷。通过在加载后1天和6天首先给予标准荧光染料骨标记并使用定量组织形态测定法评估尺骨中段的骨切片来测量骨形成。左侧非负载尺骨作为内部控制的负载的影响。在ER-β−/−和野生型（WT）小鼠中，机械负荷增加了尺骨中段骨膜骨表面的骨形成率。男性ER-β−/−与男性相比，尺骨对负荷的反应相似。WT小鼠，但对于雌性小鼠，ER-β−/−小鼠更有效地刺激骨形成（P< 0.001）。我们的结论是，雌激素信号通过ER-β抑制长骨骨膜表面的机械负荷反应。
Mechanical loading caused by physical activity can stimulate bone formation and strengthen the skeleton. Estrogen receptors (ERs) play some role in the signaling cascade that is initiated in bone cells after a mechanical load is applied. We hypothesized that one of the ERs, ER-β, influences the responsiveness of bone to mechanical loads. To test our hypothesis, 16-wk-old male and female mice with null mutations in ER-β (ER-β−/−) had their right forelimbs subjected to short daily loading bouts. The loading technique used has been shown to increase bone formation in the ulna. Each loading bout consisted of 60 compressive loads within 30 s applied daily for 3 consecutive days. Bone formation was measured by first giving standard fluorochrome bone labels 1 and 6 days after loading and using quantitative histomorphometry to assess bone sections from the midshaft of the ulna. The left nonloaded ulna served as an internal control for the effects of loading. Mechanical loading increased bone formation rate at the periosteal bone surface of the mid-ulna in both ER-β−/−and wild-type (WT) mice. The ulnar responsiveness to loading was similar in male ER-β−/−vs. WT mice, but for female mice bone formation was stimulated more effectively in ER-β−/−mice (P< 0.001). We conclude that estrogen signaling through ER-β suppresses the mechanical loading response on the periosteal surface of long bones.