Pathobiological Functions of PGF2á on human dental pulp cells

Objective:Previous studies have found that amount of PGF2a in human dental pulp raises during inflammation. However the roles and the effects of PGF2a in human dental pulp are not fully clear. The aim of this research was to evaluate the effects of PGF2a on human dental pulp cells in vitro. Methods:reverse transcriptase polymerase chain reaction (RT-PCR);western blotting;Sircol Collagen Assay;alkaline phosphatase (ALK-P)staining were used for this study. Results:We found that primary human dental pulp cells expressed FP receptor as analyzed by RT-PCR. Activation of FP receptor by PGF2a (10 uM) induced both ERK and CREB phosphorylation in pulp cells as shown in western blotting. Exposure to different concentration of PGF2a (0.1, 0.5, 1, 10, 25 uM) declined the collagen content of pulp cells as analyzed by Sircol Collagen Assay. PGF2a (> 1 uM) also decreased the ALK-P activity and mRNA expression. However, U0126, SQ22536 and H89 (inhibitors of MEK1. adenylate cyclase and protein kinase A (PKA), respectively) could not prevent the PGF2a- attenuated ALK-P activity in dental pulp cells. Conclusions:These results indicate that PGF2a may activate FP receptors leading to ERK/CREB activation during its production in inflamed pulp. PGF2a attenuated the collagen turnover and ALK-P activity of pulp cells possibly via pathways other than ERK/CREB and adenylate cyclase/PKA activation. PGF2a is suggested as a crucial factor in pulpal inflammation by regulation the pulp cell behavior.