The present study attempted to identify potential key genes and pathways of peri-implantitis, and to investigate the possible mechanisms associated with it. An array data of GSE57631 was downloaded, including six samples of peri-implantitis tissue and two samples of normal tissue from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) in the peri-implantitis samples compared with normal ones were analyzed with the limma package. Moreover, Gene Ontology annotation and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses for DEGs were performed by DAVID. A protein-protein interaction (PPI) network was established using Cytoscape software, and significant modules were analyzed using Molecular Complex Detection. A total of 819 DEGs (759 upregulated and 60 downregulated) were identified in the peri-implantitis samples compared with normal ones. Moreover, the PPI network was constructed with 413 nodes and 1,114 protein pairs. Heat shock protein HSP90AA1 (90 kDa α, member 1), a hub node with higher node degrees in module 4, was significantly enriched in antigen processing, in the presentation pathway and nucleotide-binding oligomerization domain (NOD)-like receptor-signaling pathway. In addition, nuclear factor-κ-B1 (NFKB1) was enriched in the NOD-like receptor-signaling pathway in KEGG pathway enrichment analysis for upregulated genes. The proteasome is the most significant pathway in module 1 with the highest P-value. Therefore, the results of the present study suggested that HSP90AA1 and NFKB1 may be potential key genes, and the NOD-like receptor signaling pathway and proteasome may be potential pathways associated with peri-implantitis development.
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.
Background Peri-implantitis of tooth seriously affects the life quality of patients. This study aims 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 Used Pg-LPS (0.1, 1, 10 µg/mL) to construct an inflammatory model of HGFs, and transfected HSP90AA1-siRNA to construct HSP90AA1 low expression HGFs cell line, respectively. After that, cell viability, the contents of IL-1β, IL-6, TNF-α were detected by CCK-8, and ELISA assay. Intracellular ROS, the expressions of HSP90α, HSP90β were detected by immunofluorescence. Apoptosis was detected by flow cytometry. Western blot, RT-PCR detected the protein and gene level of HSP90AA1, and relative protein expressions of p-NF-κB p65/NF-κB p65, LC3 II/I, ATG5, and Beclin-1 was detected by western blot. Results In the inflammatory cell model, compared with the control group, Pg-LPS did not affect cell viability, increased the contents of IL-1β, IL-6, and TNF-α in cells, and increased protein, gene level of HSP90AA1, and p-NF-κB p65/NF-κB p65, LC3 II/I, ATG5, Beclin-1 protein levels. In HGFs cell line with low expression of HSP90AA1, compared with siNC group, the levels of inflammatory factors, ROS, apoptosis rate, HSP90α, HSP90β protein expression, and autophagy related protein levels in siHSP90AA1 group were significantly reduced. Conclusions This study confirmed that HSP90AA1 gene promotes Pg-LPS induced HGFs inflammation mediated by autophagy in vitro. It is suggested that HSP90AA1 is a key gene in the development of peri-implantitis.
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