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HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy

BACKGROUND: Peri-implantitis of tooth seriously affects the life quality of patients. This study aimed to investigate the role of HSP90AA1 in the inflammatory of human gingival fibroblasts (HGFs) induced by porphyromonas gingivalis lipopolysaccharide (Pg-LPS), and to provide a potential therapeutic...

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Autores principales: Zhang, Huang, Huang, Jie, Fan, XuSheng, Miao, RuiJing, Wang, YongWu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9419417/
https://www.ncbi.nlm.nih.gov/pubmed/36028869
http://dx.doi.org/10.1186/s12903-022-02304-0
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author Zhang, Huang
Huang, Jie
Fan, XuSheng
Miao, RuiJing
Wang, YongWu
author_facet Zhang, Huang
Huang, Jie
Fan, XuSheng
Miao, RuiJing
Wang, YongWu
author_sort Zhang, Huang
collection PubMed
description BACKGROUND: Peri-implantitis of tooth seriously affects the life quality of patients. This study aimed to investigate the role of HSP90AA1 in the inflammatory of human gingival fibroblasts (HGFs) induced by porphyromonas gingivalis lipopolysaccharide (Pg-LPS), and to provide a potential therapeutic target for clinical treatment of peri-implantitis. METHODS: Pg-LPS (0.1, 1, 10 μg/mL) was used to construct the inflammatory model of HGFs to evaluate the effect of Pg-LPS on HGFs. Then HSP90AA1-siRNA was transfected to construct HSP90AA1 low expression HGFs cell line, and 3-MA was also added. After that, cell viability, apoptosis, the contents of inflammatory cytokines were detected by CCK-8, flow cytometry and ELISA assay, respectively. Intracellular ROS, the expressions of HSP90α, HSP90β were detected by immunofluorescence. The levels of HSP90AA1, p-NF-κB p65/NF-κB p65, LC3 II/I, ATG5, Beclin-1 and TLR protein were detected by western blot. RESULTS: Pg-LPS treatment didn’t affect the viability of HGFs cells, but induced the cell apoptosis and ROS generation, increased the contents of IL-1β, IL-6, TNF-α, and the protein expressions of HSP90AA1, p-NF-κBp65/NF-κBp65, LC3II/I, ATG5, and Beclin-1 in HGFs. While HSP90AA1-siRNA transfected into Pg-LPS induced HGFs significantly reduced the HSP90AA1, HSP90α, HSP90β expression, decreased the inflammatory factors, ROS generation, cell apoptosis rate, and autophagy-related proteins and TLR2/4 protein levels. What’s more, the addition of autophagy inhibitor 3-MA further promote the effect of HSP90AA1-siRNA on Pg-LPS treated HGFs. CONCLUSIONS: This study showed that HSP90AA1 promoted the inflammatory response of Pg-LPS induced HGFs by regulating autophagy. The addition of 3-MA further confirmed that autophagy may mediate siHSP90AA1 to enhance the inflammatory response. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12903-022-02304-0.
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spelling pubmed-94194172022-08-28 HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy Zhang, Huang Huang, Jie Fan, XuSheng Miao, RuiJing Wang, YongWu BMC Oral Health Research BACKGROUND: Peri-implantitis of tooth seriously affects the life quality of patients. This study aimed to investigate the role of HSP90AA1 in the inflammatory of human gingival fibroblasts (HGFs) induced by porphyromonas gingivalis lipopolysaccharide (Pg-LPS), and to provide a potential therapeutic target for clinical treatment of peri-implantitis. METHODS: Pg-LPS (0.1, 1, 10 μg/mL) was used to construct the inflammatory model of HGFs to evaluate the effect of Pg-LPS on HGFs. Then HSP90AA1-siRNA was transfected to construct HSP90AA1 low expression HGFs cell line, and 3-MA was also added. After that, cell viability, apoptosis, the contents of inflammatory cytokines were detected by CCK-8, flow cytometry and ELISA assay, respectively. Intracellular ROS, the expressions of HSP90α, HSP90β were detected by immunofluorescence. The levels of HSP90AA1, p-NF-κB p65/NF-κB p65, LC3 II/I, ATG5, Beclin-1 and TLR protein were detected by western blot. RESULTS: Pg-LPS treatment didn’t affect the viability of HGFs cells, but induced the cell apoptosis and ROS generation, increased the contents of IL-1β, IL-6, TNF-α, and the protein expressions of HSP90AA1, p-NF-κBp65/NF-κBp65, LC3II/I, ATG5, and Beclin-1 in HGFs. While HSP90AA1-siRNA transfected into Pg-LPS induced HGFs significantly reduced the HSP90AA1, HSP90α, HSP90β expression, decreased the inflammatory factors, ROS generation, cell apoptosis rate, and autophagy-related proteins and TLR2/4 protein levels. What’s more, the addition of autophagy inhibitor 3-MA further promote the effect of HSP90AA1-siRNA on Pg-LPS treated HGFs. CONCLUSIONS: This study showed that HSP90AA1 promoted the inflammatory response of Pg-LPS induced HGFs by regulating autophagy. The addition of 3-MA further confirmed that autophagy may mediate siHSP90AA1 to enhance the inflammatory response. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12903-022-02304-0. BioMed Central 2022-08-26 /pmc/articles/PMC9419417/ /pubmed/36028869 http://dx.doi.org/10.1186/s12903-022-02304-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Zhang, Huang
Huang, Jie
Fan, XuSheng
Miao, RuiJing
Wang, YongWu
HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title_full HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title_fullStr HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title_full_unstemmed HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title_short HSP90AA1 promotes the inflammation in human gingival fibroblasts induced by Porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
title_sort hsp90aa1 promotes the inflammation in human gingival fibroblasts induced by porphyromonas gingivalis lipopolysaccharide via regulating of autophagy
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9419417/
https://www.ncbi.nlm.nih.gov/pubmed/36028869
http://dx.doi.org/10.1186/s12903-022-02304-0
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