Transgenic mice expressing soluble tumor necrosis factor-receptor are protected against bone loss caused by estrogen deficiency
Transgenic mice expressing soluble tumor necrosis factor-receptor are protected against bone loss caused by estrogen deficiency
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DOI：
10.1172/jci119333
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发表时间：
1997-04-01
影响因子：
15.9
通讯作者：
Garcia, I
中科院分区：
文献类型：
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作者：
Ammann, P;Rizzoli, R;Garcia, I
为探讨肿瘤坏死因子(TNF-α)在雌激素缺乏所致的骨丢失中的作用，对6个月龄表达高血中和肿瘤坏死因子-I型可溶性肿瘤坏死因子受体(STNFR1)-FcIgG3融合蛋白的转基因小鼠和对照仔鼠进行了卵巢切除的研究。这些转基因小鼠在骨量(通过骨矿密度和含量评估)和强度方面与对照组小鼠相同。卵巢切除12周后，转基因小鼠骨量减少，骨转换标志物骨钙素升高，与假手术小鼠无明显差异，提示肿瘤坏死因子α在雌激素缺乏所致骨丢失的发病机制中起重要作用。
To evaluate the role of tumor necrosis factor (TNF alpha) in bone loss resulting from estrogen deficiency, the effects of ovariectomy were explored in six-month-old transgenic mice expressing high blood levels of a soluble TNF receptor type I (sTNFR1)-FcIgG3 fusion protein, which neutralizes TNF alpha, and in their nontransgenic littermates used as controls. These transgenic mice were identical to control mice in bone mass (evaluated by bone mineral density and content) and strength. 12 weeks after ovariectomy, the decrease in bone mass and increase in osteocalcin (marker of bone turnover) found in control mice were not observed in transgenic mice, which were not different from sham-operated mice, transgenic or not, This observation suggests a critical role for TNF alpha in the pathogenesis of bone loss induced by estrogen deficiency, a common cause of morbidity in postmenopausal women.