PROSTAGLANDIN E-2 STIMULATES SODIUM-DEPENDENT PHOSPHATE-TRANSPORT IN OSTEOBLASTIC CELLS VIA A PROTEIN-KINASE C-MEDIATED PATHWAY

Eicosanoids are released by bone cells in response to physical, hormon al, and cytokine stimulation, and they can both inhibit and stimulate bone formation. We investigated the effect of PGE, on sodium-dependent phosphate (Na,Pi) transport in a rat bone-derived cell line, PyMS. PG E(2) and 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of protein kinase C, increased Na(d)Pi uptake in a dose-and time-dependen t manner. There was no change in Na-dependent alanine transport, and t he effects of PGE(2) and TPA were not associated with corresponding ch anges in cell number or protein content. Their effects on Na(d)Pi upta ke were not additive. Calphostin C, an inhibitor of protein kinase C ( 10(-8) hr) completely blocked TPA-and PGE(2)-stimulated Na(d)Pi uptake . The results are consistent with a crucial role of protein kinase C a ctivation in the short term stimulation of Na(d)Pi transport by PGE(2) in PyMS cells.