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The effect of 24,25 dihydroxyvitamin D 3 on calcium efflux: the role of protein kinase C
Author(s) -
DRANITZKIELHALEL Michal,
WALD Hanna,
SPRAGUE Stuart,
POPOVTZER Mordecai M
Publication year - 1998
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1046/j.1440-1797.1998.d01-26.x
Subject(s) - protein kinase c , efflux , calcium , endocrinology , medicine , cytosol , phorbol , vitamin d and neurology , signal transduction , biochemistry , chemistry , enzyme
SUMMARY: 24,25 dihydroxyvitamin D 3 (24,25(OH) 2 D 3 ) is more abundant than 1,25(OH) 2 D 3 in the serum. 1,25 dihydroxyvitamin D 3 , 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) 2 D 3 affects calcium flux in bone, neonatal rat calvaria were cultured and the effect of 24,25(OH) 2 D 3 on calcium flux and signal transduction pathways were evaluated. Compared with a control, 24,25(OH) 2 D 3 (10 8 mol/L) inhibited basal net calcium efflux. 24,25 dihydroxyvitamin D 3 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) 2 D 3 . However, 24,25(OH) 2 D 3 had no effect on cyclic AMP (cAMP) production. In conclusion, 24,25(OH) 2 D 3 has a direct effect on bone by inhibiting net calcium efflux which is probably mediated by the deactivation of PKC.