scholarly journals STAT1/SOCS1/3 Are Involved in the Inflammation-Regulating Effect of GAS6/AXL in Periodontal Ligament Cells Induced by Porphyromonas gingivalis Lipopolysaccharide In Vitro

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shengnan Zhang ◽  
Yingjun Liu ◽  
Xuekui Wang ◽  
Na An ◽  
Xiangying Ouyang
Keyword(s):  
Porphyromonas Gingivalis ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Inflammatory Diseases ◽  
Specific Protein ◽  
Periodontal Ligament Cells ◽  
Cytokine Signaling ◽  
Porphyromonas Gingivalis Lipopolysaccharide ◽  
Inflammatory Processes

Periodontitis involves chronic inflammation of the tissues around the teeth caused by plaque and the corresponding immune response. Growth arrest-specific protein 6 (GAS6) and AXL receptor tyrosine kinase (AXL) are known to be involved in inflammatory diseases, while signal transducer and activator of transcription-1 (STAT1) and suppressor of cytokine signaling (SOCS) are related to inflammatory processes. Moreover, miRNA34a directly targets AXL to regulate the AXL expression. However, the specific roles of GAS6 and AXL in periodontitis remain unclear. This study was designed to explore the effect and mechanism of AXL on the expression of inflammatory cytokines induced by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) in human periodontal ligament cells (hPDLCs). The effects of different concentrations of P. gingivalis LPS on the expression of GAS6/AXL in hPDLCs were observed. Additionally, the effect of LPS on AXL was investigated by transfection of the miRNA34a inhibitor. AXL was knocked down or overexpressed to observe the release of inflammatory cytokines interleukin- (IL-) 8 and IL-6. The results showed that the expression levels of GAS6 and AXL decreased after P. gingivalis LPS infection. Transfection of a miR-34a inhibitor to hPDLCs demonstrated a role of miR-34a in the downregulation of AXL expression induced by LPS. Moreover, AXL knockdown or overexpression influencing the expression of IL-8 and IL-6 was investigated under LPS stimulation. AXL knockdown decreased the expression of STAT1 and SOCS1/3. Overall, these results demonstrate that AXL inhibits the expression of LPS-induced inflammatory cytokines in hPDLCs and that STAT1 and SOCS1/3 are involved in the regulation of inflammation by GAS6/AXL.

scholarly journals Porphyromonas gingivalis lipopolysaccharide stimulation in human periodontal ligament stem cells: role of epigenetic modifications to the inflammation

2017 ◽  
Vol 61 (3) ◽  
Author(s):  
Francesca Diomede ◽  
Soundara Rajan Thangavelu ◽  
Ilaria Merciaro ◽  
Monica D'Orazio ◽  
Placido Bramanti ◽  
...  
Keyword(s):  
Stem Cells ◽  
Porphyromonas Gingivalis ◽  
Inflammatory Disease ◽  
Periodontal Ligament ◽  
Model System ◽  
Epigenetic Mechanism ◽  
Periodontal Ligament Stem Cells ◽  
Porphyromonas Gingivalis Lipopolysaccharide

<p>Periodontitis is a chronic oral inflammatory disease produced by bacteria. Gingival retraction and bone and connective tissues resorption are the hallmarks of this disease. Chronic periodontitis may contribute to the risk of onset or progression of neuroinflammatory pathological conditions, such as Alzheimer’s disease. The main goal of the present study was to investigate if the role of epigenetic modulations is involved in periodontitis using human periodontal ligament stem cells (hPDLSCs) as an <em>in vitro</em> model system. hPDLSCs were treated with lipopolysaccharide of <em>Porphyromonas gingivalis</em> and the expression of proteins associated with DNA methylation and histone acetylation, such as DNMT1 and p300, respectively, and inflammatory transcription factor NF-kB, were examined. Immunofluorescence, Western blot and next generation sequencing results demonstrated that <em>P. gingivalis </em>lipopolysaccharide significantly reduced DNA methylase DNMT1, while it markedly upregulated the level of histone acetyltransferase p300 and NF-kB in hPDLSCs. Our results showed that <em>P. gingivalis </em>lipopolysaccharide markedly regulate the genes involved in epigenetic mechanism, which may result in inflammation induction. We propose that <em>P. gingivalis </em>lipopolysaccharide-treated hPDLSCs could be a potential in vitro model system to study epigenetics modulations associated with periodontitis, which might be helpful to identify novel biomarkers linked to this oral inflammatory disease.</p>

scholarly journals Methanandamide diminish the Porphyromonas gingivalis lipopolysaccharide induced response in human periodontal ligament cells

2020 ◽  
Author(s):  
Fengqiu Zhang ◽  
Burcu Özdemir ◽  
Phuong Quynh Nguyen ◽  
Oleh Andrukhov ◽  
Xiaohui Rausch-Fan
Keyword(s):  
Porphyromonas Gingivalis ◽  
Periodontal Ligament ◽  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Periodontal Ligament Cells ◽  
Induced Response ◽  
Human Periodontal Ligament Cells ◽  
Chemotactic Protein ◽  
Improved Stability ◽  
Porphyromonas Gingivalis Lipopolysaccharide

Abstract Background: The endocannabinoid system is involved in the regulation of periodontal tissue homeostasis. Synthetic cannabinoid methanandamide (Meth-AEA) has improved stability and affinity to cannabinoid receptors compared to its endogenous analog anandamide. In the present study, we investigated the effect of methanandamide on the production of pro-inflammatory mediators in primary human periodontal ligament cells (hPdLCs).Methods: hPdLCs were treated with Meth-AEA for 24 h, and the resulting production of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 was measured in the absence or the presence of Porphyromonas gingivalis lipopolysaccharide (LPS). Additionally, the effect of Meth-AEA on the proliferation/viability of hPdLCs was measured by MTT method. Results: Methanandamide at a concentration of 10 µM significantly inhibited P. gingivalis LPS induced production of IL-6, IL-8, and MCP-1. Basal production of IL-6 and IL-8 was slightly enhanced by 10 µM Meth-AEA. No effect of Meth-AEA on the basal production of MCP-1 was observed. Meth-AEA in concentrations up to 10 µM did not affect the proliferation of hPdLCs, but significantly inhibited it at a concentration of 30 µM. Conclusion: Our study suggests that the inflammatory response in periodontal ligament cells could be influenced by the activation of the cannabinoid system, which might be potentially involved in the progression of periodontal disease.

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