Prostaglandins E(2) and F(2alpha) enhance differentiation of cementoblastic cells.
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.


CONCLUSIONS
We conclude that PGE(2) and PGF(2alpha) exert an anabolic effect on OCCM mineralization through activation of PKC signaling.
Camargo
P M
PM
Section of Periodontics, Division of Associated Clinical Specialties, School of Dentistry, University of California, Los Angeles, CA 90095, USA.
Lagos
R
R
Pirih
F Q M
FQ
Benitez
A
A
Nervina
J M
JM
Tetradis
S
S
D002113:Calcification, Physiologic / Q000187:drug effects*; D002461:Cell Line, Transformed; D003739:Dental Cementum / Q000166:cytology / Q000187:drug effects*; D015237:Dinoprost / Q000494:pharmacology*; D015232:Dinoprostone / Q000494:pharmacology*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology; D011982:Receptors, Prostaglandin / Q000819:agonists; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D011461:Prostaglandins F, Synthetic; D011982:Receptors, Prostaglandin; C006326:fluprostenol; D015237:Dinoprost; D015232:Dinoprostone; D013755:Tetradecanoylphorbol Acetate