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Can ultrasound counteract bone loss? Effect of low-intensity ultrasound stimulation on a model of osteoclastic precursor

机译:超声波可以抵消骨质流失吗?低强度超声刺激对破骨细胞前体模型的影响

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The aim of the present work is to determine whether mechanical stress caused by ultrasound (US) exposure affects osteoclastic precursor cells, thus addressing the hypothesis that mechanical strain-induced perturbation of preosteoclastic cell machinery can contribute to the occurrence of bone turnover alterations. Moreover, cell cytoskeleton was studied because of its supposed involvement in cell mechanotransduction. Our experimental model was the FLG 29.1 human cell line, previously characterized as an osteoclastic precursor model. Cell proliferation was quantified by trypan blue exclusion assay. Cell morpho-functional state was monitored by multispectral imaging autofluorescence microscopy. The expression of cytoskeletal components and markers of proliferation (Ki67) and osteoclastic differentiation (RANK) was analysed by immunocytochemistry. The findings demonstrated that US stimulation affects FLG 29.1 cell growth, depresses the expression of cytoskeletal components and markers of proliferation and differentiation, induces cell damage, thus supporting the hypothesis that US exposure inhibits osteoclastogenesis. These results have been compared with those obtained previously by exposure of FLG 29.1 cells to modelled hypogravity conditions. Finally, the possibility to utilize US stimulation for counteracting osteoporosis has been discussed.
机译:本工作的目的是确定由超声(US)暴露引起的机械应力是否影响破骨细胞前体细胞,从而解决假说:机械应变引起的前破骨细胞机制的扰动可导致骨转换改变的发生。此外,由于细胞骨架被认为参与细胞机械转导,因此对其进行了研究。我们的实验模型是FLG 29.1人类细胞系,以前被称为破骨细胞前体模型。通过锥虫蓝排除试验定量细胞增殖。通过多光谱成像自发荧光显微镜监测细胞形态功能状态。通过免疫细胞化学分析细胞骨架成分的表达和增殖(Ki67)和破骨细胞分化(RANK)的标志。这些发现表明,US刺激会影响FLG 29.1细胞的生长,抑制细胞骨架成分的表达以及增殖和分化的标志物,诱导细胞损伤,从而支持US暴露抑制破骨细胞形成的假说。将这些结果与先前通过将FLG 29.1细胞暴露于模拟的重力环境中获得的结果进行了比较。最后,讨论了利用US刺激对抗骨质疏松症的可能性。

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