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Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death

The NOD-like receptor protein 3/caspase-1 inflammasome can be activated in human dental pulp tissue and fibroblasts; however, the underlying mechanisms are poorly understood. In the present study, lipopolysaccharide (LPS) was used to treat dental pulp cells to establish an inflammation model. Cell v...

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Autores principales: Gao, Yang, You, Xinran, Liu, Yubo, Gao, Fei, Zhang, Yuan, Yang, Jianrong, Yang, Chen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027320/
https://www.ncbi.nlm.nih.gov/pubmed/32104285
http://dx.doi.org/10.3892/etm.2020.8475
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author Gao, Yang
You, Xinran
Liu, Yubo
Gao, Fei
Zhang, Yuan
Yang, Jianrong
Yang, Chen
author_facet Gao, Yang
You, Xinran
Liu, Yubo
Gao, Fei
Zhang, Yuan
Yang, Jianrong
Yang, Chen
author_sort Gao, Yang
collection PubMed
description The NOD-like receptor protein 3/caspase-1 inflammasome can be activated in human dental pulp tissue and fibroblasts; however, the underlying mechanisms are poorly understood. In the present study, lipopolysaccharide (LPS) was used to treat dental pulp cells to establish an inflammation model. Cell viability was examined by sulforhodamine B assay. Interleukin (IL)-1β, caspase-1, microtubule-associated protein-1 light chain 3-II/I and p62 were determined by western blotting and ELISA. The phosphorylation (p-) levels of NF-κB and NF-κB inhibitor (IκB)α protein were observed by western blotting. The results demonstrated that LPS induced pyroptotic cell death in cultured dental pulp cells, which was supported by the increased levels of IL-1β, IL-18 and caspase-1. Rapamycin and 3-methyladenine (3-MA) were used to activate and inhibit autophagy, and it was observed that LPS increased autophagy and rapamycin reduced LPS-induced dental pulp cell pyroptosis. However, 3-MA aggravated LPS-induced dental pulp cell pyroptosis. In addition, LPS inhibited the expression of IκBα, but increased the expression of p-NF-κB. Compared with the LPS group, 3-MA further inhibited the expression of IκBα but promoted the expression of p-NF-κB. However, rapamycin produced the opposite results to LPS. Under LPS treatment, the NF-κB pathway inhibitor BAY11-7082 further enhanced the inhibitory effects of rapamycin, but inhibited the promoting effects of 3-MA on the protein expression levels of IL-1β and caspase-1. The results of the present study demonstrated that there is an important crosstalk between autophagy, pyroptosis and the NF-κB pathway, and that the modulation of pyroptosis in dental pulp cells may be a promising strategy to pulpitis therapy.
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spelling pubmed-70273202020-02-26 Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death Gao, Yang You, Xinran Liu, Yubo Gao, Fei Zhang, Yuan Yang, Jianrong Yang, Chen Exp Ther Med Articles The NOD-like receptor protein 3/caspase-1 inflammasome can be activated in human dental pulp tissue and fibroblasts; however, the underlying mechanisms are poorly understood. In the present study, lipopolysaccharide (LPS) was used to treat dental pulp cells to establish an inflammation model. Cell viability was examined by sulforhodamine B assay. Interleukin (IL)-1β, caspase-1, microtubule-associated protein-1 light chain 3-II/I and p62 were determined by western blotting and ELISA. The phosphorylation (p-) levels of NF-κB and NF-κB inhibitor (IκB)α protein were observed by western blotting. The results demonstrated that LPS induced pyroptotic cell death in cultured dental pulp cells, which was supported by the increased levels of IL-1β, IL-18 and caspase-1. Rapamycin and 3-methyladenine (3-MA) were used to activate and inhibit autophagy, and it was observed that LPS increased autophagy and rapamycin reduced LPS-induced dental pulp cell pyroptosis. However, 3-MA aggravated LPS-induced dental pulp cell pyroptosis. In addition, LPS inhibited the expression of IκBα, but increased the expression of p-NF-κB. Compared with the LPS group, 3-MA further inhibited the expression of IκBα but promoted the expression of p-NF-κB. However, rapamycin produced the opposite results to LPS. Under LPS treatment, the NF-κB pathway inhibitor BAY11-7082 further enhanced the inhibitory effects of rapamycin, but inhibited the promoting effects of 3-MA on the protein expression levels of IL-1β and caspase-1. The results of the present study demonstrated that there is an important crosstalk between autophagy, pyroptosis and the NF-κB pathway, and that the modulation of pyroptosis in dental pulp cells may be a promising strategy to pulpitis therapy. D.A. Spandidos 2020-03 2020-01-28 /pmc/articles/PMC7027320/ /pubmed/32104285 http://dx.doi.org/10.3892/etm.2020.8475 Text en Copyright: © Gao et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Gao, Yang
You, Xinran
Liu, Yubo
Gao, Fei
Zhang, Yuan
Yang, Jianrong
Yang, Chen
Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title_full Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title_fullStr Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title_full_unstemmed Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title_short Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
title_sort induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027320/
https://www.ncbi.nlm.nih.gov/pubmed/32104285
http://dx.doi.org/10.3892/etm.2020.8475
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