Prostaglandins E2 and F2α Enhance Differentiation of Cementoblastic Cells.

<bold>Background: </bold>The prostaglandins (PG) E2 and PGF2α are important cytokines in periodontal physiology and pathology. PGE2 and PGF2α alter cell function by binding and activating the plasmamembrane G-protein-coupled PG receptors. In this study, we examined the PGE2 and PGF2α effects on the immortalized cementoblastic OCCM cells.<bold>Methods: </bold>Confluent OCCM cells were treated with PGE2 , PGF2α , specific activators/inhibitors of the EP prostanoid receptors, a specific activator of the FP prostanoid receptor, and direct activators/inhibitors of the protein kinase C (PKC) signaling pathway. Mineral nodule formation was assessed by the von Kossa stain.<bold>Results: </bold>PGE2 and PGF2α significantly increased mineralization of OCCM cells. The EP1 and EP3 PG receptor activators 16,16-dimethyl-prostaglandin E2 and sulprostone, also increased mineralization. In contrast, specific activators of the EP2 or the EP2/EP3/EP4 receptors did not have any effect. Fluprostenol, a specific activator of the FP receptor, significantly increased mineralization of OCCM cells. FP and EP (1 or 3) receptors signal through activation of the protein kinase C (PKC) pathway. Indeed, phorbol 12-myristate 13-acetate (PMA), a direct activator of the PKC pathway, significantly increase OCCM mineralization, while pre-treatment of OCCM cells with the PKC inhibitor GF109203× (bisindolylmaleimide) significantly decreased mineralization.<bold>Conclusion: </bold>We conclude that PGE2 and PGF2α exert an anabolic effect on OCCM mineralization through activation of PKC signaling. J Periodontol 2005;76:303-309. [ABSTRACT FROM AUTHOR]