BMC oral health · 2017
The effect of chlormadinone acetate on odontogenic differentiation of human dental pulp cells: in vitro study.
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Kim Se-Min, Lee Bin-Na, Koh Jeong-Tae, Chang Hoon-Sang, Hwang In-Nam, Oh Won-Mann, Min Kyung-San, Hwang Yun-Chan
Аннотация
BACKGROUND: Chlormadinone acetate (CMA) is a derivative of progesterone and is used as an oral contraceptive. The aim of this study was to investigate the effects of CMA on odontogenic differentiation and mineralization of human dental pulp cells (hDPCs) and related signaling pathways.
METHODS: Cell viability was determined by the water-soluble tetrazolium (WST)-1 assay. Odontogenic differentiation of hDPCs was evaluated by real-time polymerase chain reaction using odontogenic marker genes, such as alkaline phosphatase (ALP), osteocalcin (OCN), dentin sialophosphoprotein (DSPP), and dentin matrix protein-1 (DMP-1). Mineralization of hDPCs was evaluated by ALP staining and alizarin red staining. The extracellular signal-regulated kinase (ERK) pathway was examined by Western blot analysis.
RESULTS: There was no statistically significant difference in cell viability between the control and CMA-treated groups. Our analysis of odontogenic marker genes indicated that CMA enhanced the expression of those genes. CMA-treated hDPCs showed increased ALP activity and formation of mineralized nodules, compared with control-treated cells. In addition, CMA stimulation resulted in phosphorylation of ERK and resulted in inhibition of downstream molecules by the ERK inhibitor U0126.
CONCLUSIONS: These findings suggest that CMA improves odontogenic differentiation and mineralization of hDPCs through the ERK signaling pathway.
METHODS: Cell viability was determined by the water-soluble tetrazolium (WST)-1 assay. Odontogenic differentiation of hDPCs was evaluated by real-time polymerase chain reaction using odontogenic marker genes, such as alkaline phosphatase (ALP), osteocalcin (OCN), dentin sialophosphoprotein (DSPP), and dentin matrix protein-1 (DMP-1). Mineralization of hDPCs was evaluated by ALP staining and alizarin red staining. The extracellular signal-regulated kinase (ERK) pathway was examined by Western blot analysis.
RESULTS: There was no statistically significant difference in cell viability between the control and CMA-treated groups. Our analysis of odontogenic marker genes indicated that CMA enhanced the expression of those genes. CMA-treated hDPCs showed increased ALP activity and formation of mineralized nodules, compared with control-treated cells. In addition, CMA stimulation resulted in phosphorylation of ERK and resulted in inhibition of downstream molecules by the ERK inhibitor U0126.
CONCLUSIONS: These findings suggest that CMA improves odontogenic differentiation and mineralization of hDPCs through the ERK signaling pathway.
Предметные рубрики MeSH
Alkaline PhosphataseCalcification, PhysiologicCell DifferentiationCell SurvivalChlormadinone AcetateContraceptives, Oral, SyntheticDental PulpExtracellular Matrix ProteinsExtracellular Signal-Regulated MAP KinasesHumansOdontoblastsOsteocalcinPhosphoproteinsPhosphorylationRNA, MessengerSialoglycoproteinsDentin Sialophosphoprotein