Osteopetrosis in mice lacking NF-κB1 and NF-κB2
Author: ["Violetta Iotsova","Jorge Caamaño","James Loy","Yi Yang","Anne Lewin","Rodrigo Bravo"]
Publication: Nature Medicine
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Abstract
The nfkbl and nfkb2 genes encode closely related products regulating immune and inflammatory responses1–3. Their role during development and differentiation remains unclear. The generation of nfkb1 null mice (p50−/−) resulted in altered immune responses, but had no effect on development4. Similarly, nfkb2 knockout mice (p52−/−) did not show developmental defects (J.C. et al., manuscript submitted). We have investigated the potential for in vivo compensatory functions of these genes by generating double-knockout mice. The surprising result was that the animals developed osteopetrosis because of a defect in osteoclast differentiation, suggesting redundant functions of NF-κB1 and NF-κB2 proteins in the development of this cell lineage. The osteopetrotic phenotype was rescued by bone marrow transplantation, indicating that the hematopoietic component was impaired. These results define a new mouse osteopetrotic mutant and implicate NF-κB proteins in bone development, raising new directions in the treatment of bone disorders.
Cite this article
Iotsova, V., Caamaño, J., Loy, J. et al. Osteopetrosis in mice lacking NF-κB1 and NF-κB2. Nat Med 3, 1285–1289 (1997). https://doi.org/10.1038/nm1197-1285