Transgenic mice expressing soluble tumor necrosis factor-receptor are protected against bone loss caused by estrogen deficiency

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 alp...

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Bibliographic Details
Published in:The Journal of clinical investigation 1997-04, Vol.99 (7), p.1699-1703
Main Authors: Ammann, P, Rizzoli, R, Bonjour, J P, Bourrin, S, Meyer, J M, Vassalli, P, Garcia, I
Format: Article
Language:English
Subjects:
Animals
Bone Density
Estrogens - deficiency
Female
Interleukin-1 - physiology
Interleukin-6 - physiology
Mice
Mice, Inbred BALB C
Mice, Transgenic
Osteoporosis - prevention & control
Ovariectomy
Receptors, Tumor Necrosis Factor - physiology
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Summary: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.
ISSN:0021-9738
DOI:10.1172/jci119333