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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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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. |
format | Online Article Text |
id | pubmed-7027320 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
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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