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首页> 外文期刊>Journal of Cellular Physiology >Schnurri-2 deficiency counteracts against bone loss induced by ovariectomy.
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Schnurri-2 deficiency counteracts against bone loss induced by ovariectomy.

机译：对骨Schnurri-2不足抵消卵巢切除术引起的损失。

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摘要

Schnurri (Shn)-2 is a transcriptional modulator of bone formation and bone resorption and its deficiency causes low turnover state with higher cancellous bone mass due to the defects in osteoclasts that exceeds the defects in osteoblasts in mice. We addressed whether such low turnover of bone remodeling in Shn2 deficiency may be modulated in the absence of estrogen that induces high turnover state in vivo. Ovariectomy reduced bone mass in wild type compared to sham operated control mice and such reduction in bone mass was also observed in Shn2 deficient mice. However, due to the high levels of basal bone mass in Shn2 deficient mice, the bone mass levels after ovariectomy were still comparable to sham operated wild-type mice. Analysis indicated that estrogen depletion increased bone resorption at similar levels in wild type and Shn2 deficient mice though the basal levels of osteoclast number was slightly lower in Shn2-deficient mice. In contrast, basal levels of bone marrow cell mineralization in cultures were low in Shn2-deficeint mice while estrogen depletion increased the mineralization levels to those that were comparable to sham wild type. This indicates that Shn2-deficient mice maintain bone mass at the levels comparable to wild-type sham mice even after ovariectomy-induced bone loss and this correlates with the high levels of mineralization activity in bone marrow cells after ovariectomy.
机译：Schnurri (Shn) 2是一个转录调制器骨形成和骨吸收和它缺乏会导致较低的人员流动率较高的国家松质骨质量的缺陷破骨细胞,超过了缺陷成骨细胞在小鼠体内。低周转率Shn2骨重塑缺乏可能调制在缺乏雌激素诱导高营业额状态vivo而虚假的操作控制老鼠等减少骨量Shn2也观察到有缺陷的老鼠。Shn2缺陷小鼠的基底骨量卵巢切除术后骨密度水平仍在与虚假的野生型老鼠。分析表明雌激素消耗增加骨吸收在相似的水平野生型和Shn2虽然有缺陷的老鼠基础水平的破骨细胞数量略低Shn2-deficient老鼠。的骨髓细胞矿化水平文化很低在Shn2-deficeint老鼠雌激素消耗增加了矿化那些与虚假的野生的水平类型。保持在水平与骨密度即使在野生型虚假的老鼠ovariectomy-induced骨质流失和这个有关与高水平的矿化活动在卵巢切除术后骨髓细胞。

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