1α,25-dihydroxyvitamin D3 increases TGF β1 binding to human osteoblasts

David Nagel, Rajiv Kumar

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

1β,25-Dihydroxyvitamin D3 (1α,25(OH)2D3) increases the binding of transforming growth factor β1(TGF β1) via TGF β receptors to the surface of human osteoblasts. The increase in TGF β receptors induced by 1α,25(OH)2D3 is dependent on increases in TGF β secretion induced by 1α,25(OH)2D3, since antibodies directed against TGF β block the increase in TGF β1 binding. The increase in TGF β type I and II receptors on cell surfaces following 1α,25(OH)2D3 treatment is associated with increases in receptor mRNA concentrations. Increases in receptor mRNA concentrations following 1α,25(OH)2D3 treatment are not due to changes in receptor gene transcription. The role of TGF β receptors, in mediating the growth responses to 1α,25(OH)2D3 is demonstrated by showing that osteoblasts which express dominant negative, kinase-deficient TGF β type II receptors, fail to respond to the growth-inhibitory effects of 1α,25(OH)2D3. An increase in TGF β receptor expression is important in mediating 1α,25(OH)2D3-associated changes in the growth rate of osteoblasts.

Original languageEnglish (US)
Pages (from-to)1558-1563
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume290
Issue number5
DOIs
StatePublished - 2002

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Keywords

  • 1α,25-dihydroxyvitamin D
  • Cellular growth
  • Osteoblasts
  • TGF β receptors
  • Transforming growth factor β

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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