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Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells

INTRODUCTION: Smoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs). METHODS: DPSCs were treated with va...

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Autores principales: Hardin, Leyla Tahrani, Vang, David, Thor, Der, Han, Xiaoyuan, Mashkoor, Fatima, Alpagot, Tamer, Ojcius, David M., Xiao, Nan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: European Publishing on behalf of the International Society for the Prevention of Tobacco Induced Diseases (ISPTID) 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10392041/
https://www.ncbi.nlm.nih.gov/pubmed/37533959
http://dx.doi.org/10.18332/tid/168125
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author Hardin, Leyla Tahrani
Vang, David
Thor, Der
Han, Xiaoyuan
Mashkoor, Fatima
Alpagot, Tamer
Ojcius, David M.
Xiao, Nan
author_facet Hardin, Leyla Tahrani
Vang, David
Thor, Der
Han, Xiaoyuan
Mashkoor, Fatima
Alpagot, Tamer
Ojcius, David M.
Xiao, Nan
author_sort Hardin, Leyla Tahrani
collection PubMed
description INTRODUCTION: Smoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs). METHODS: DPSCs were treated with various doses of cigarette smoke condensate (CSC) or nicotine. Cell proliferation and survival were evaluated by a water-soluble tetrazolium salt (WST-1) and a survival assay. DPSC migration, cytokine expression, mutagenesis, and the signaling pathway were also measured during CSC and nicotine treatment. RESULTS: Low concentrations of CSC and nicotine did not impair cell proliferation, but higher concentrations reduced cell proliferation. CSC and nicotine could impede DPSC survival and migration in a dose-dependent manner. In addition, the cytokine secretion expression profile was altered with CSC or nicotine treatments. In particular, secretion of IL-6, TNF-α, and IL-10 significantly increased, while TGF-β1 levels showed different patterns after exposure to CSC or nicotine, as shown by ELISA and quantitative PCR. Nicotine treatment increased AKT (also known as protein kinase B) and extracellular signal-regulated kinase (ERK) phosphorylation. Finally, CSC induced higher levels of mutagenicity than nicotine, as shown by the Ames test. CONCLUSIONS: These findings suggest that cigarette smoke exposure alters the regenerative abilities of DPSCs in various ways. Future studies are warranted to further characterize the underlying molecular mechanisms of smoking-mediated damage to DPSCs, which will guide the personalized stem cell treatment plan for smoking patients.
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spelling pubmed-103920412023-08-02 Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells Hardin, Leyla Tahrani Vang, David Thor, Der Han, Xiaoyuan Mashkoor, Fatima Alpagot, Tamer Ojcius, David M. Xiao, Nan Tob Induc Dis Research Paper INTRODUCTION: Smoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs). METHODS: DPSCs were treated with various doses of cigarette smoke condensate (CSC) or nicotine. Cell proliferation and survival were evaluated by a water-soluble tetrazolium salt (WST-1) and a survival assay. DPSC migration, cytokine expression, mutagenesis, and the signaling pathway were also measured during CSC and nicotine treatment. RESULTS: Low concentrations of CSC and nicotine did not impair cell proliferation, but higher concentrations reduced cell proliferation. CSC and nicotine could impede DPSC survival and migration in a dose-dependent manner. In addition, the cytokine secretion expression profile was altered with CSC or nicotine treatments. In particular, secretion of IL-6, TNF-α, and IL-10 significantly increased, while TGF-β1 levels showed different patterns after exposure to CSC or nicotine, as shown by ELISA and quantitative PCR. Nicotine treatment increased AKT (also known as protein kinase B) and extracellular signal-regulated kinase (ERK) phosphorylation. Finally, CSC induced higher levels of mutagenicity than nicotine, as shown by the Ames test. CONCLUSIONS: These findings suggest that cigarette smoke exposure alters the regenerative abilities of DPSCs in various ways. Future studies are warranted to further characterize the underlying molecular mechanisms of smoking-mediated damage to DPSCs, which will guide the personalized stem cell treatment plan for smoking patients. European Publishing on behalf of the International Society for the Prevention of Tobacco Induced Diseases (ISPTID) 2023-08-01 /pmc/articles/PMC10392041/ /pubmed/37533959 http://dx.doi.org/10.18332/tid/168125 Text en © 2023 Tahrani Hardin L. et al. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License.
spellingShingle Research Paper
Hardin, Leyla Tahrani
Vang, David
Thor, Der
Han, Xiaoyuan
Mashkoor, Fatima
Alpagot, Tamer
Ojcius, David M.
Xiao, Nan
Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title_full Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title_fullStr Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title_full_unstemmed Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title_short Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
title_sort cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10392041/
https://www.ncbi.nlm.nih.gov/pubmed/37533959
http://dx.doi.org/10.18332/tid/168125
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