Rosiglitazone Inhibits Proliferation and Induces Osteopontin Gene Expression in Human Dental Pulp Cells

• We evaluated the roles of rosiglitazone on pulp repair.
• Rosiglitazone significantly decreased cell proliferation.
• Rosiglitazone did not affect cell viability and apoptosis or necrosis.
• Rosiglitazone accelerated calcified nodule formation.
• Rosiglitazone significantly increased osteopontin gene expression.

IntroductionRosiglitazone (RSG) is a synthetic full agonist of transcription factor peroxisome proliferator activated receptor gamma. Previous studies have suggested an anti-inflammatory effect of RSG on lipopolysaccharide-induced pulp inflammation. However, its role in other cellular events related to pulp repair has not been investigated. Therefore, the aim of the present study was to evaluate the effect of RSG on human dental pulp cell viability, proliferation, migration, and osteoblastic/odontoblastic differentiation.MethodsCell proliferation was evaluated by [3H]-thymidine assay. Cell viability was assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay and by measuring the percentage of apoptotic cells by flow cytometry. Cell migration was estimated by scratch wound healing assay. Mineralization and cell differentiation were evaluated by alizarin red S staining and real-time polymerase chain reaction gene expression assay, respectively.ResultsRSG significantly decreased cell proliferation and did not have effect on cell viability, apoptosis/necrosis, or migration. Alizarin red S showed that RSG accelerated calcified nodule formation. Results of real-time polymerase chain reaction demonstrated that RSG upregulated osteopontin expression, whereas expression of dentin sialophosphoprotein, dentin matrix protein-1, and osteocalcin was not affected.ConclusionsThese findings suggest that RSG decreases human dental pulp cell proliferation, while positively regulating osteopontin expression.