The Effects of Dexamethasone, Ascorbic Acid, and β-Glycerophosphate on Osteoblastic Differentiation by Regulating Estrogen Receptor and Osteopontin Expression

• Published in: The Journal of surgical research Vol. 173; no. 1; pp. 99 - 104
• Main Author: Park, Jun-Beom, D.D.S., Ph.D
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2012
• Subjects: Alkaline Phosphatase - metabolism; Animals; ascorbic acid; Ascorbic Acid - pharmacology; Calcification, Physiologic - drug effects; Cell Differentiation - drug effects; Cell Line; Cell Proliferation - drug effects; Cell Survival - drug effects; Cells, Cultured; dexamethasone; Dexamethasone - pharmacology; differentiation; Dose-Response Relationship, Drug; Glycerophosphates - pharmacology; Mice; mineralization; Models, Animal; osteoblast; Osteoblasts - cytology; Osteoblasts - drug effects; Osteoblasts - metabolism; Osteopontin - metabolism; Phenotype; Receptors, Estrogen - metabolism; Surgery; Transforming Growth Factor beta - metabolism; β-glycerophosphate; dexamethasone; β-glycerophosphate; ascorbic acid; mineralization; differentiation; osteoblast
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/j.jss.2010.09.010

Background Ascorbic acid (AA), β-glycerophosphate (GP), and dexamethasone (DEX) are the compounds known to favor the expression of the osteoblastic phenotype in several bone cell systems. Materials and Methods In this report, the combination effects of differentiation agents on osteoprecursor cells were evaluated. The effect on cell proliferation was determined by a cell viability test with morphologic analysis. Differentiation and mineralization were evaluated using an alkaline phosphatase activity test and alizarin red-S staining. Protein expressions related to bone formation, such as transforming growth factor-beta (TGF-β), estrogen receptor-alpha (ER-α), and osteopontin (OPN) were evaluated by using a Western blot analysis. Results and Conclusion AA and GP provided an inductive effect for differentiation of osteoprecusor cells, while short-term application of DEX seemed to lead to a dose-dependent increase of cellular differentiation. Long-term use of DEX seemed to reduce mineralization. These effects may seem to be regulated by the expression of ER-α, OPN, and TGF-β. Further studies related to this mechanism within the in vivo model may be necessary to ascertain greater detail.