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首页> 外文期刊>Journal of Cellular Physiology >Mechanical loading stimulates the release of transforming growth factor-beta activity by cultured mouse calvariae and periosteal cells.
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Mechanical loading stimulates the release of transforming growth factor-beta activity by cultured mouse calvariae and periosteal cells.

机译：机械负荷刺激的释放转化生长因子的活动培养老鼠calvariae和骨膜细胞。

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We have shown earlier that mechanical stimulation by intermittent hydrostatic compression (IHC) inhibits bone resorption and stimulates bone formation in cultured fetal mouse calvariae (Klein-Nulend et al., 1986, Arthritis Rheum., 29: 1002-1009). The production of soluble bone factors by such calvariae is also modified (Klein-Nulend et al., 1993, Cell Tissue Res., 271:513-517). Transforming growth factor-beta (TGF-beta) is an important local regulator of bone metabolism and is produced by osteoblasts. In this study, the release of TGF-beta activity as a result of mechanical stress was examined in organ cultures of neonatal mouse calvariae, in primary cultures of calvariae-derived osteoprogenitor (OPR) cells, and in more differentiated osteoblastic (OB) cells. Whole calvariae and calvariae-derived cells were cultured in the presence or absence of IHC for 1-7 days and medium concentrations of active as well as total TGF-beta were measured using a bioassay. IHC (maximum 13 kPa, maximal pressure rate 32.5 kPa/sec) was generated by intermittently (0.3 Hz) compressing the gas phase above the cultures. We found that mechanical loading by IHC stimulated the release of TGF-beta activity from cultured calvariae by twofold after 1 day. IHC also stimulated the release of TGF-beta activity from calvariae-derived cells after 1 and 3 days. The absolute amounts of TGF-beta activity released were lower in OPR cells than in OB cells, but the stimulatory effect of IHC was greater in OPR cells. Total TGF-beta (active and bound) released into the medium was not affected by IHC. IHC did not change the dry weight of the organ cultures, nor the DNA or protein content of the cell cultures. These data show that mechanical perturbation of bone cells, particularly OPR cells, enhances the activation of released TGF-beta. We conclude that modulation of TGF-beta metabolism may be part of the response of bone tissue to mechanical stress.
机译：早些时候,我们已经表明机械刺激通过间歇流体静力压缩(包含IHC)抑制骨吸收,刺激骨骼形成培养胎儿calvariae老鼠1002 - 1009)。因素等calvariae也修改271:513 - 517)。(及)是一个重要的地方监管机构骨代谢,由成骨细胞。在这项研究中,释放及活动由于机械应力是检查新生儿鼠标calvariae的机关文化的主要文化calvariae-derivedosteoprogenitor(超载比)细胞,和更多分化成骨细胞的细胞(OB)。calvariae calvariae-derived细胞培养在包含IHC的存在与否1 - 7天,中等浓度的活跃总测量及使用生物测定。生成率32.5 kPa /秒)间歇性地(0.3赫兹)压缩气相以上文化。加载包含IHC刺激及释放的从培养calvariae活动两个方面1天。从calvariae-derived细胞及活动1和3天后。及活动发布在超载比低细胞比OB细胞,但刺激在超载比细胞包含IHC效应更大。及(活跃和绑定)释放到中没有包含IHC影响。改变器官的干重文化,也没有细胞的DNA或蛋白质含量的文化。这些数据表明,机械扰动骨细胞,特别是超载比细胞,增强了激活及发布。调制及代谢的可能的一部分骨组织的机械应力的响应。

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