Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling

Long-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of huma...

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Main Authors: Wei Qin, Qi-Ting Huang, Michael D. Weir, Zhi Song, Ashraf F. Fouad, Zheng-Mei Lin, Liang Zhao, Hockin H. K. Xu
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2017/8717454
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author Wei Qin
Qi-Ting Huang
Michael D. Weir
Zhi Song
Ashraf F. Fouad
Zheng-Mei Lin
Liang Zhao
Hockin H. K. Xu
author_facet Wei Qin
Qi-Ting Huang
Michael D. Weir
Zhi Song
Ashraf F. Fouad
Zheng-Mei Lin
Liang Zhao
Hockin H. K. Xu
author_sort Wei Qin
collection DOAJ
description Long-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of human dental pulp cells (DPCs) is unknown. Whether EtOH affects the odontoblastic differentiation of DPCs through the mechanistic target of rapamycin (mTOR) remains unexplored. The objective of this study was to investigate the effects of EtOH on DPC differentiation and mineralization. DPCs were isolated and purified from human dental pulps. The proliferation and odontoblastic differentiation of DPCs treated with EtOH were subsequently investigated. Different doses of EtOH were shown to be cytocompatible with DPCs. EtOH significantly activated the mTOR pathway in a dose-dependent manner. In addition, EtOH downregulated the alkaline phosphatase activity, attenuated the mineralized nodule formation, and suppressed the expression of odontoblastic markers including ALP, DSPP, DMP-1, Runx2, and OCN. Moreover, the pretreatment with rapamycin, a specific mTOR inhibitor, markedly reversed the EtOH-induced odontoblastic differentiation and cell mineralization. Our findings show for the first time that EtOH can suppress DPC differentiation and mineralization in a mTOR-dependent manner, indicating that EtOH may be involved in negatively regulating the dental pulp repair.
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spelling doaj-art-998af08dfc8d4ab08691a9f7e066af722025-02-03T01:32:29ZengWileyStem Cells International1687-966X1687-96782017-01-01201710.1155/2017/87174548717454Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR SignalingWei Qin0Qi-Ting Huang1Michael D. Weir2Zhi Song3Ashraf F. Fouad4Zheng-Mei Lin5Liang Zhao6Hockin H. K. Xu7Department of Operative Dentistry and Endodontics, Guanghua School of Stomatology, Sun Yat-sen University and Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, ChinaDepartment of Operative Dentistry and Endodontics, Guanghua School of Stomatology, Sun Yat-sen University and Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, ChinaBiomaterials and Tissue Engineering Division, Department of Endodontics, Periodontics and Prosthodontics, University of Maryland School of Dentistry, Baltimore, MD 21201, USADepartment of Operative Dentistry and Endodontics, Guanghua School of Stomatology, Sun Yat-sen University and Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, ChinaDepartment of Endodontics, School of Dentistry, University of North Carolina, Chapel Hill, NC 27599-7450, USADepartment of Operative Dentistry and Endodontics, Guanghua School of Stomatology, Sun Yat-sen University and Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, ChinaBiomaterials and Tissue Engineering Division, Department of Endodontics, Periodontics and Prosthodontics, University of Maryland School of Dentistry, Baltimore, MD 21201, USABiomaterials and Tissue Engineering Division, Department of Endodontics, Periodontics and Prosthodontics, University of Maryland School of Dentistry, Baltimore, MD 21201, USALong-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of human dental pulp cells (DPCs) is unknown. Whether EtOH affects the odontoblastic differentiation of DPCs through the mechanistic target of rapamycin (mTOR) remains unexplored. The objective of this study was to investigate the effects of EtOH on DPC differentiation and mineralization. DPCs were isolated and purified from human dental pulps. The proliferation and odontoblastic differentiation of DPCs treated with EtOH were subsequently investigated. Different doses of EtOH were shown to be cytocompatible with DPCs. EtOH significantly activated the mTOR pathway in a dose-dependent manner. In addition, EtOH downregulated the alkaline phosphatase activity, attenuated the mineralized nodule formation, and suppressed the expression of odontoblastic markers including ALP, DSPP, DMP-1, Runx2, and OCN. Moreover, the pretreatment with rapamycin, a specific mTOR inhibitor, markedly reversed the EtOH-induced odontoblastic differentiation and cell mineralization. Our findings show for the first time that EtOH can suppress DPC differentiation and mineralization in a mTOR-dependent manner, indicating that EtOH may be involved in negatively regulating the dental pulp repair.http://dx.doi.org/10.1155/2017/8717454
spellingShingle Wei Qin
Qi-Ting Huang
Michael D. Weir
Zhi Song
Ashraf F. Fouad
Zheng-Mei Lin
Liang Zhao
Hockin H. K. Xu
Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
Stem Cells International
title Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
title_full Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
title_fullStr Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
title_full_unstemmed Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
title_short Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling
title_sort alcohol inhibits odontogenic differentiation of human dental pulp cells by activating mtor signaling
url http://dx.doi.org/10.1155/2017/8717454
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