P53 Functions As a Negative Regulator of Osteoblastogenesis, Osteoblast-dependent Osteoclastogenesis, and Bone Remodeling.
From: The Institute of Molecular and Cell Biology, Singapore 138673.
The Journal of cell biology
- Publish Date: Jan 2006
- ISSN: 0021-9525
- Volume: 172
- Issue: 1
- Pages: 115-25
- Medium: Print
- Language: English
- Citation (JAMA): Wang Xueying, Kua Hui-Yi, Hu Yuanyu, et al. P53 Functions As a Negative Regulator of Osteoblastogenesis, Osteoblast-dependent Osteoclastogenesis, and Bone Remodeling.. J. Cell Biol. Jan 2006;172:115-25
Abstract
p53 is a well known tumor suppressor. We show that p53 also regulates osteoblast differentiation, bone formation, and osteoblast-dependent osteoclast differentiation. Indeed, p53(-/-) mice display a high bone mass phenotype, and p53(-/-) osteoblasts show accelerated differentiation, secondary to an increase in expression of the osteoblast differentiation factor osterix, as a result. Reporter assays indicate that p53 represses osterix transcription by the minimal promoter in a DNA-binding-independent manner. In addition, p53(-/-) osteoblasts have an enhanced ability to favor osteoclast differentiation, in association with an increase in expression of macrophage-colony stimulating factor, which is under the control of osterix. Furthermore, inactivating p53 is sufficient to rescue the osteoblast differentiation defects observed in mice lacking c-Abl, a p53-interacting protein. Thus, these results identify p53 as a novel regulator of osteoblast differentiation, osteoblast-dependent osteoclastogenesis, and bone remodeling.
Mesh Headings (Keywords): Animals, Bone Remodeling, Cell Differentiation, Cell Proliferation, Cells, Cultured, Female, Macrophage Colony-Stimulating Factor, Male, Mice, Mice, Knockout, Osteoblasts, Osteoclasts, Proto-Oncogene Proteins c-abl, Transcription Factors, Tumor Suppressor Protein p53, Up-Regulation
Check for Full Text / PubMed Unique Identifier (PMID): 16380437
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