Transgenic mice expressing soluble tumor necrosis factor-receptor are protected against bone loss caused by estrogen deficiency
Autor: | S. Bourrin, René Rizzoli, Irène Garcia, Pierre Vassalli, Jean-Marc Meyer, Jean-Philippe Bonjour, Patrick Ammann |
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Rok vydání: | 1997 |
Předmět: |
Genetically modified mouse
medicine.medical_specialty Bone density medicine.drug_class Ovariectomy Transgene Osteoporosis Mice Transgenic ddc:616.07 Interleukin-6/physiology Receptors Tumor Necrosis Factor Bone remodeling Pathogenesis Mice Bone Density Internal medicine medicine Animals Bone mineral Mice Inbred BALB C biology Interleukin-6 business.industry Obstetrics and Gynecology Estrogens General Medicine medicine.disease Estrogens/*deficiency Endocrinology Estrogen Osteocalcin biology.protein Female Interleukin-1/physiology Tumor necrosis factor alpha Osteoporosis/*prevention & control business Receptors Tumor Necrosis Factor/*physiology Research Article Interleukin-1 |
Zdroj: | Journal of Clinical Investigation, Vol. 99, No 7 (1997) pp. 1699-1703 |
ISSN: | 0021-9738 |
DOI: | 10.1172/jci119333 |
Popis: | 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. |
Databáze: | OpenAIRE |
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