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1,25-dihydroxyvitamin D3 inhibits Osteocalcin expression in mouse through an indirect mechanism

R Zhang1, P Ducy, G Karsenty

  • 1Department of Molecular Genetics, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

Insights

In mice, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) inhibits osteocalcin gene expression by preventing transcription factor binding, unlike in rats and humans. This occurs indirectly, impacting genes upstream of osteocalcin.

Area of Science:

  • Molecular Biology
  • Genetics
  • Endocrinology

Background:

  • 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is crucial for mineral metabolism and osteoblast gene regulation.
  • In rats and humans, 1,25-(OH)2D3 enhances osteocalcin expression via vitamin D-responsive elements.
  • Osteocalcin is a key protein in bone mineralization and remodeling.

Purpose of the Study:

  • To investigate the effect of 1,25-(OH)2D3 on osteocalcin gene expression in mice.
  • To elucidate the regulatory mechanism of 1,25-(OH)2D3 on osteocalcin genes (OG1 and OG2) in mouse osteoblasts.

Main Methods:

  • Primary osteoblast cultures and whole-animal studies in mice.
  • DNA transfection assays and DNA binding experiments.
  • Analysis of transcription factor binding to cis-acting elements (OSE2) in gene promoters.

Main Results:

  • 1,25-(OH)2D3 inhibited both OG1 and OG2 expression in mouse osteoblasts and in vivo.
  • No functional vitamin D-responsive element was identified in the promoters of OG1 or OG2.
  • 1,25-(OH)2D3 treatment reduced the binding of OSF2 to the OSE2 element in OG1 and OG2 promoters.
  • Mutation of the OSE2 element abolished the inhibitory effect of 1,25-(OH)2D3.

Conclusions:

  • 1,25-(OH)2D3 exhibits species-specific regulation of osteocalcin gene expression.
  • In mice, 1,25-(OH)2D3 inhibits osteocalcin expression through an indirect mechanism involving OSF2 binding to OSE2.
  • This regulation highlights the complexity of vitamin D signaling in bone metabolism.

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