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Parathyroid hormone, prostaglandin E2, and 1,25-dihydroxyvitamin D3 decrease the level of Na+-Ca2+ exchange protein

N S Krieger1

  • 1Department of Medicine, Box 675, University of Rochester School of Medicine, 601 Elmwood Avenue, Rochester, New York 14642, USA.

Calcified Tissue International
|May 1, 1997
PubMed
Summary

Parathyroid hormone (PTH), prostaglandin E2 (PGE2), and 1,25(OH)2D3 reduce Na+-Ca2+ exchanger protein levels in osteoblasts. This explains how these hormones inhibit Na+-dependent Ca2+ transport in bone cells.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Osteoblasts regulate bone metabolism through calcium (Ca2+) transport.
  • Na+-Ca2+ exchange is a key mechanism for Ca2+ transport in osteoblasts.
  • Hormonal regulation of Na+-Ca2+ exchange activity has been previously observed.

Purpose of the Study:

  • To investigate the molecular mechanism underlying the inhibition of Na+-Ca2+ exchange by calcemic agents in osteoblasts.
  • To determine if hormonal inhibition affects Na+-Ca2+ exchanger protein synthesis or levels.

Main Methods:

  • Osteoblastic rat osteosarcoma cells (UMR-106) were treated with parathyroid hormone (PTH), prostaglandin E2 (PGE2), or 1,25(OH)2D3.
  • Plasma membrane proteins were isolated and analyzed using immunoblot analysis with an antibody against the Na+-Ca2+ exchanger.

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  • Protein levels were quantified and compared between treated and untreated cells.

    • Main Results:

    • A specific Na+-Ca2+ exchanger protein band (90 kD) was detected in UMR-106 cell membranes.
    • Treatment with PTH, PGE2, or 1,25(OH)2D3 significantly decreased the levels of this Na+-Ca2+ exchanger protein.
    • PTH inhibition was dose-dependent and time-dependent, with maximal effect at 10(-7) M and 16-24 hours.

    Conclusions:

    • Osteoblastic cells express a protein that cross-reacts with antibodies to the cardiac Na+-Ca2+ exchanger.
    • The inhibition of Na+-Ca2+ exchange activity by PTH, PGE2, and 1,25(OH)2D3 is mediated by a reduction in exchanger protein levels.
    • These findings highlight a novel regulatory mechanism for Ca2+ transport in bone cells.