The effect of 24,25 dihydroxyvitamin D3 on calcium efflux: The role of protein kinase C

Michal Dranitzki-Elhalel*, Hanna Wald, Stuart Sprague, Mordecai M. Popovtzer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


24,25 dihydroxyvitamin D3 (24,25(OH)2D3) is more abundant than 1,25(OH)2D3 in the serum. 1,25 dihydroxyvitamin D3, a potent calciotropic metabolite of vitamin D, has been shown to induce calcium efflux from bone. This action is probably mediated, in part, by protein kinase C (PKC). To determine whether 24,25(OH)2D3 affects calcium flux in bone, neonatal rat calvaria were cultured and the effect of 24,25(OH)2D3 on calcium flux and signal transduction pathways were evaluated. Compared with a control, 24,25(OH)2D3 (108 mol/L) inhibited basal net calcium efflux. 24,25 dihydroxyvitamin D3 also inhibited net calcium efflux induced by the phorbol ester 12 Myristate 13-Acetate (PMA). Translocation of PKC from the membrane to the cytosolic fraction was rapidly and transiently induced by 24,25(OH)2D3. However, 24,25(OH)2D3 had no effect on cyclic AMP (cAMP) production. In conclusion, 24,25(OH)2D3 has a direct effect on bone by inhibiting net calcium efflux which is probably mediated by the deactivation of PKC.

Original languageAmerican English
Pages (from-to)157-162
Number of pages6
Issue number3
StatePublished - 1998
Externally publishedYes


  • 24,25(OH)D
  • Bone
  • Calcium flux
  • Cyclic AMP
  • Metabolism
  • Protein kinase C


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