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• W2891534760 endingPage "139" @default.
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• W2891534760 abstract "Lipopolysaccharide (LPS) is a major component of cell wall in gram-negative bacteria and has been proved to be a predominant pathogenic factor in periodontitis. Porphyromonas gingivalis (P.g) was abundant in patients with periodontitis and was associated with patient clinic-pathological characteristics. Furthermore, autophagy is a potential mechanism in inflammatory disease. In this study, we hypothesized that LPS from P.g may affect the physiological functions of human gingival fibroblasts (HGFs) through activating cellular autophagy. However, it remains unclear what molecular basis related to LPS-induced autophagy in HGFs. Here, we initially addressed the contribution of LPS from P.g in inducing autophagy in HGFs. Through a combination of morphology and quantification approaches involving autophagosomes formation observation as well as microtubule-associated protein light chain 3 (LC3)-II conversion. We further evaluated whether the PI3K/Akt/mTOR signaling could mediate LPS-induced autophagy in HGFs. Our results revealed that autophagy was more obvious in LPS-treated cells compared with that in control groups. Finally, our results demonstrated that LPS from P.g promoted autophagy in HGFs and was negatively regulated by PI3K/Akt/mTOR. Analysis of these data implicates that LPS from P.g has a significant impact on the autophagy of HGFs by suppressing PI3K/Akt/mTOR signaling pathway." @default.
• W2891534760 created "2018-09-27" @default.
• W2891534760 creator A5046897135 @default.
• W2891534760 creator A5048216847 @default.
• W2891534760 creator A5070389870 @default.
• W2891534760 creator A5086366375 @default.
• W2891534760 date "2018-10-01" @default.
• W2891534760 modified "2023-10-14" @default.
• W2891534760 title "Lipopolysaccharide from Porphyromonas gingivalis promotes autophagy of human gingival fibroblasts through the PI3K/Akt/mTOR signaling pathway" @default.
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• W2891534760 doi "https://doi.org/10.1016/j.lfs.2018.09.023" @default.
• W2891534760 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30218719" @default.
• W2891534760 hasPublicationYear "2018" @default.
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