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Updated: Aug 11, 2026
A Novel Culture Model for Human Pluripotent Stem Cell Propagation on Gelatin in Placenta-conditioned Media
Published on: August 3, 2015
Prostaglandins E(2) and F(2alpha) enhance differentiation of cementoblastic cells
P M Camargo1, R Lagos, F Q M Pirih
1Section of Periodontics, Division of Associated Clinical Specialties, School of Dentistry, University of California, Los Angeles, CA 90095, USA.
Background:
The prostaglandins (PG) E(2) and PGF(2alpha) are important cytokines in periodontal physiology and pathology. PGE(2) and PGF(2alpha) alter cell function by binding and activating the plasmamembrane G-protein-coupled PG receptors. In this study, we examined the PGE(2) and PGF(2alpha) effects on the immortalized cementoblastic OCCM cells.
Methods:
Confluent OCCM cells were treated with PGE(2), PGF(2alpha), 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.
Results:
PGE(2) and PGF(2alpha) significantly increased mineralization of OCCM cells. The EP1 and EP3 PG receptor activators 16,16-dimethyl-prostaglandin E(2) 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 GF109203x (bisindolylmaleimide) significantly decreased mineralization.
Conclusion:
We conclude that PGE(2) and PGF(2alpha) exert an anabolic effect on OCCM mineralization through activation of PKC signaling.
