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Cited by 39Oral microbiology and periodontitis researchDental Implant Techniques and OutcomesHeat shock proteins research

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

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Zhang, Huang, Huang, Jie, Fan, XuSheng, Miao, RuiJing, Wang, YongWu·2022·BMC Oral Health
DOI 10.1186/s12903-022-02304-0PMC PMC9419417
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Abstract

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.

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Authors
Zhang, H., Huang, J., Fan, X., Miao, R., & Wang, Y.
Affiliations
Zhejiang University (CN)
Corresponding author
Wang, YongWu
ORCID
Venue
BMC Oral Health
Publisher
Springer Science and Business Media LLC
Published
2022-08-26
Volume
22
Issue
1
Pages
366-366
ISSN
1472-6831 (ISSN-L)
DOI
10.1186/s12903-022-02304-0
PMC
PMC9419417
OpenAlex
W4293677686
Cited by
39
References
46
Citations by year
2026: 7 · 2025: 15 · 2024: 9 · 2023: 7 · 2022: 1
FWCI
7.98
Type
journal article
Language
en
Open access
Licence
Locations
  • BMC Oral Health (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Medical and public health projects of Zhejiang Province (2021432823)
Topics
  • Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
  • Health Sciences › Dentistry › Oral Surgery › Dental Implant Techniques and Outcomes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
HSP90AA1, Porphyromonas gingivalis, lipopolysaccharide, gingival fibroblasts, peri-implantitis, inflammation, autophagy, NF-κB signaling, reactive oxygen species, apoptosis, TLR2/4, HSP90α, HSP90β, 3-methyladenine
MeSH terms
Beclin-1, Autophagy, Cells, Cultured, Fibroblasts, Gingiva, Humans, Inflammation, Lipopolysaccharides, NF-kappa B, Porphyromonas gingivalis, Reactive Oxygen Species, HSP90 Heat-Shock Proteins, RNA, Small Interfering, Peri-Implantitis

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