c-Fos: A Key Regulator of Osteoclast-Macrophage Lineage Determination and Bone Remodeling

Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1994-10, Vol.266 (5184), p.443-448
Main Authors: Grigoriadis, Agamemnon E., Wang, Zhao-Qi, Cecchini, Marco G., Hofstetter, Willy, Felix, Rolf, Fleisch, Herbert A., Wagner, Erwin F.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Bone marrow
Bone Marrow Transplantation
Bone Remodeling - physiology
Bone resorption
Bones
Capsules
Cell Differentiation
Cells, Cultured
Fundamental and applied biological sciences. Psychology
Genes, fos
Hematopoietic Stem Cell Transplantation
Hematopoietic stem cells
Hematopoietic Stem Cells - cytology
Macrophages
Macrophages - cytology
Mice
Mice, Mutant Strains
Osteoclasts
Osteoclasts - cytology
Osteogenesis
Osteopetrosis
Osteopetrosis - metabolism
Osteopetrosis - pathology
Progenitor cells
Proto-Oncogene Proteins c-fos - genetics
Proto-Oncogene Proteins c-fos - physiology
Proto-oncogenes
Skeleton and joints
Space life sciences
Spleen cells
Stromal cells
Vertebrates: osteoarticular system, musculoskeletal system
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Summary:Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression overcame this differentiation block. The lack of Fos also caused a lineage shift between osteoclasts and macrophages that resulted in increased numbers of bone marrow macrophages. These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.7939685