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The Sox2 high mobility group transcription factor inhibits mature osteoblast function in transgenic mice
Greg Holmes1, Timothy G Bromage, Claudio Basilico
1Department of Microbiology, New York University School of Medicine, 550 1st Ave, New York, NY 10016, USA.
Abstract:
We have previously shown that in osteoblasts Sox2 expression can be induced by Fgfs, and can inhibit Wnt signaling and differentiation. Furthermore, in mice in which Sox2 is conditionally deleted in the osteoblastic lineage, bones are osteopenic, and Sox2 inactivation in cultured osteoblasts leads to a loss of proliferative ability with a senescent phenotype. To help understand the role of Sox2 in osteoblast development we have specifically expressed Sox2 in bone from a Col1α1 promoter, which extended Sox2 expression into more mature osteoblasts. In long bones, trabecular cartilage remodeling was delayed and the transition from endochondral to cortical bone was disrupted, resulting in porous and undermineralized cortical bone. Collagen deposition was disorganized, and patterns of osteoclast activity were altered. Calvarial bones were thinner and parietal bones failed to develop the diploic space. Microarray analysis showed significant up- or downregulation of a variety of genes coding for non-collagenous extracellular matrix proteins, with a number of genes typical of mature osteoblasts being downregulated. Our results position Sox2 as a negative regulator of osteoblast maturation in vivo.
Insights
Sox2 acts as a negative regulator of osteoblast maturation. Overexpressing Sox2 in bone disrupts bone development, leading to porous, undermineralized bone and altered gene expression in osteoblasts.
Area of Science:
- Bone Biology
- Developmental Biology
- Genetics
Background:
- Sox2 is induced by Fgfs in osteoblasts, inhibiting Wnt signaling and differentiation.
- Conditional deletion of Sox2 in osteoblasts leads to osteopenia and senescence.
- Understanding Sox2's role in osteoblast development is crucial for bone health.
Purpose of the Study:
- To investigate the in vivo role of Sox2 in osteoblast maturation.
- To examine the effects of Sox2 overexpression in bone using a Col1α1 promoter.
Main Methods:
- Generation of transgenic mice with Sox2 overexpression driven by the Col1α1 promoter.
- Analysis of long bone and calvarial bone phenotypes.
- Microarray analysis to assess gene expression changes in osteoblasts.
Main Results:
- Overexpression of Sox2 delayed trabecular cartilage remodeling and disrupted the endochondral to cortical bone transition.
- Resulting cortical bone was porous and undermineralized, with disorganized collagen deposition and altered osteoclast activity.
- Calvarial bones were thinner, and parietal bones lacked diploic space; microarray revealed downregulation of mature osteoblast genes.
Conclusions:
- Sox2 functions as a negative regulator of osteoblast maturation in vivo.
- Altered Sox2 levels significantly impact bone structure, mineralization, and extracellular matrix gene expression.
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