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EBF2 Regulates Osteoblast-Dependent Differentiation of Osteoclasts

MPG-Autoren
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Kieslinger,  Matthias
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Folberth,  Stephanie
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Dobreva,  Gergana
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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https://www.sciencedirect.com/science/article/pii/S1534580705003916?via%3Dihub
(Verlagsversion)

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Zitation

Kieslinger, M., Folberth, S., Dobreva, G., Dorn, T., Croci, L., Erben, R., et al. (2005). EBF2 Regulates Osteoblast-Dependent Differentiation of Osteoclasts. Developmental Cell, 9, 757-767. doi:10.1016/j.devcel.2005.10.009.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002B-9303-3
Zusammenfassung
Communication between bone-depositing osteoblasts and bone-resorbing osteoclasts is required for bone development and homeostasis. Here, we identify EBF2, a member of the early B cell factor (EBF) family of transcription factors that is expressed in osteoblast progenitors, as a regulator of osteoclast differentiation. We find that mice homozygous for a targeted inactivation of Ebf2 show reduced bone mass and an increase in the number of osteoclasts. These defects are accompanied by a marked downregulation of the osteoprotegerin (Opg) gene, encoding a RANK decoy receptor. EBF2 binds to sequences in the Opg promoter and transactivates the Opg promoter in synergy with the Wnt-responsive LEF1/TCF:β-catenin pathway. Taken together, these data identify EBF2 as a regulator of RANK-RANKL signaling and osteoblast-dependent differentiation of osteoclasts.