Dental pulp tissue is a highly vascularized tissue. One of the keys to success in vital pulp therapy is ensuring that the dental pulp is in healthy environment while maintaining good pulpal vasculature. Prostacyclin (PGI2), a physiologic vasodilating agent, has a biogenic property by enhancing angiogenesis and cellular proliferation. PGI2 and vascular endothelial growth factor (VEGF) are strongly related in many cell types and promoted vascular proliferation, yet the studies of the relationships between these two molecules are limited.In this study, we aimed to investigate the role of PGI2 to dental pulp tissue in the promotion of vascularization in human dental pulp cells (HDPC).
Methods: Human dental pulp cells were cultured in routine culture with or without prostacyclin analog, iloprost, and the production of VEGF was evaluated by ELISA and quantitative real-time PCR.
Results:
Iloprost significantly stimulated VEGF mRNA levels and protein release in a dose-dependent manner. These effects were blocked by the PGI2antagonist (CAY10449). Moreover, the basic fibroblast growth factor (bFGF) is believed to be an important factor in the process of wound healing in pathological conditions, also in the healing of pulp/dentin complex regeneration. Our study showed that pre-treatment of b-FGF inhibitor (SU-5402) prior to iloprost could inhibit VEGF production in HDPC.
Conclusions:
In conclusion, our current study suggested that prostacyclin is part of a bidirectional signaling network between the vascularization and the proliferation of the dental pulp tissue. Prostacyclin analogs, therefore, have the potential to modulate the maintenance of the dental pulp microcirculation, thus could be used as an adjuvant for drug delivery treatment for promoting and regenerating of dental pulp tissues.