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首页> 外文期刊>Journal of orthopaedic research >Pertussis toxin-sensitive G proteins as mediators of stretch-induced decrease in nitric-oxide release of osteoblast-like cells.
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Pertussis toxin-sensitive G proteins as mediators of stretch-induced decrease in nitric-oxide release of osteoblast-like cells.

机译：百日咳毒素敏感的G蛋白可作为牵张介质诱导成骨样细胞一氧化氮释放减少。

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摘要

Mechanical loading plays an important role in regulating bone remodeling, and nitric oxide may be one regulator of this process. To determine how mechanical stress modulates osteoblast function, we loaded cyclic tensile stretch on osteoblast-like cells and measured levels of nitric oxide in the medium. High frequency of stretch at any magnitude inhibited release of nitric oxide; however, low frequency of stretch enhanced its release from the static control. To examine the involvement of G protein (guanine nucleotide-binding regulatory protein) in stress-inhibited release of nitric oxide, we added pertussis toxin, a specific inhibitor of the Gi class, and found that it completely reversed the stress-inhibited release. These data support the idea that pertussis toxin-sensitive G protein is activated in the presence of cyclic tensile stretch.
机译：机械负荷在调节骨骼重塑中起着重要作用，而一氧化氮可能是这一过程的调节剂。为了确定机械应力如何调节成骨细胞的功能，我们在成骨细胞样细胞上加载了周期性拉伸，并测量了培养基中一氧化氮的水平。任何程度的高频率拉伸都会抑制一氧化氮的释放;然而，低频率的拉伸增强了它从静态控制中的释放。为了检查G蛋白（鸟嘌呤核苷酸结合调节蛋白）在压力抑制一氧化氮释放中的作用，我们添加了百日咳毒素（Gi类的特异性抑制剂），发现它完全逆转了压力抑制释放。这些数据支持在循环拉伸拉伸的情况下激活百日咳毒素敏感型G蛋白的想法。

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