Deficiency of the intermediate filament synemin reduces bone mass in vivo.
Deficiency of the intermediate filament synemin reduces bone mass in vivo.
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DOI：
10.1152/ajpcell.00218.2016
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发表时间：
2016-12
期刊：
影响因子：
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通讯作者：
Megan C. Moorer;Atum M. Buo;Karla P. García-Pelagio;J. Stains;R. Bloch
中科院分区：
文献类型：
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作者：
Megan C. Moorer;Atum M. Buo;Karla P. García-Pelagio;J. Stains;R. Bloch
虽然IV型中间丝蛋白Synmin已被证明在横纹肌和神经元组织中发挥作用，但它在骨骼组织中的存在和功能尚未被描述。在这里，我们报告了在14周大的雄性小鼠中，基因消融Synmin导致骨量减少，包括股骨远端的骨小梁比例减少2倍以上，以及股骨中段横截面积的减少，这是由于骨膜和骨内周长的减少。血清骨形成标志物和静态组织形态计量学分析显示，体内成骨细胞活性和成骨细胞数量存在统计学意义上的缺陷。有趣的是，从SYNMIN缺失小鼠分离的原代成骨细胞显示出显著的成骨能力增强，伴随而来的是细胞周期蛋白D1mRNA表达的降低，这可能解释了体内观察到的成骨细胞数量的减少。总而言之，这些数据表明了Synmin在骨生理学中的一个以前未知的重要作用。
While the type IV intermediate filament protein, synemin, has been shown to play a role in striated muscle and neuronal tissue, its presence and function have not been described in skeletal tissue. Here, we report that genetic ablation of synemin in 14-wk-old male mice results in osteopenia that includes a more than 2-fold reduction in the trabecular bone fraction in the distal femur and a reduction in the cross-sectional area at the femoral middiaphysis due to an attendant reduction in both the periosteal and endosteal perimeter. Analysis of serum markers of bone formation and static histomorphometry revealed a statistically significant defect in osteoblast activity and osteoblast number in vivo. Interestingly, primary osteoblasts isolated from synemin-null mice demonstrate markedly enhanced osteogenic capacity with a concomitant reduction in cyclin D1 mRNA expression, which may explain the loss of osteoblast number observed in vivo. In total, these data suggest an important, previously unknown role for synemin in bone physiology.