| Autor: |
Se-Min Kim, Bin-Na Lee, Jeong-Tae Koh, Hoon-Sang Chang, In-Nam Hwang, Won-Mann Oh, Kyung-San Min, Yun-Chan Hwang |
| Jazyk: |
angličtina |
| Rok vydání: |
2017 |
| Předmět: |
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| Zdroj: |
BMC Oral Health, Vol 17, Iss 1, Pp 1-7 (2017) |
| Druh dokumentu: |
article |
| ISSN: |
1472-6831 |
| DOI: |
10.1186/s12903-017-0379-0 |
| Popis: |
Abstract 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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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