Evidence that estrogens modulate activity and increase the number of 1,25-dihydroxyvitamin D receptors in osteoblast-like cells (ROS 17/2.8)

Yair Liel, Sara Kraus, Joseph Levy, Shraga Shany

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87 Scopus citations

Abstract

A detailed understanding of the mechanism of action of estrogen on bones is still lacking. The present study was designed to examine possible modulation by 17β-estradiol (E2) on the effects of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and on vitamin D receptors (VDR) in the ROS 17/2.8 osteoblast-like cell line. Cells were grown in phenol-red free medium supplemented with charcoal-stripped fetal calf serum (FCS). Total cellular VDR were measured in cell homogenates after extraction with a KCl hypertonic buffer. VDR-binding capacity doubled in the presence of 10 nM E2 (16.2 ± 2.3 vs. 7.0 ± 1.3 fmol/mg protein, respectively; P < 0.01), while the Kd for 1,25-(OH)2D3 did not change (∼0.1 nM). Tamoxifen alone had no effect on VDR, while it completely abolished the E2-induced increase in VDR, indicating that the effect was specific for E2 and estrogen receptor mediated. 1,25-(OH)2D3 inhibited cell proliferation, determined by [3H] thymidine incorporation to DNA, in a dose-dependent fashion between 0.01-100 nM. The inhibitory effect of 1,25-(OH)2D3 on cell proliferation was significantly augmented in the presence of E2 (10 nM). 1,25-(OH)2D3 increased osteocalcin secretion to the medium by the cells in a dose-dependent fashion between 0.01-100 nM. In the presence of E2 (10 nM), maximal osteocalcin secretion in response to 1,25-(OH)2D3 was 3.5-fold higher than that in response to 1,25-(OH)2D3 alone. These results indicate that E2 modulates 1,25-(OH)2D3 activity in osteoblast-like cells, and that this effect can be attributed to an increase in VDR.

Original languageEnglish
Pages (from-to)2597-2601
Number of pages5
JournalEndocrinology
Volume130
Issue number5
StatePublished - 1 Jan 1992
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology

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