scholarly journals Knockdown of TRIM52 alleviates LPS-induced inflammatory injury in human periodontal ligament cells through the TLR4/NF-κB pathway

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Peng Liu ◽  
Lijun Cui ◽  
Lifang Shen
Keyword(s):  
Signaling Pathway ◽  
Periodontal Ligament ◽  
Caspase 3 ◽  
Quantitative Polymerase Chain Reaction ◽  
Periodontal Ligament Cells ◽  
Inflammatory Injury ◽  
Human Periodontal Ligament Cells ◽  
Diphenyltetrazolium Bromide ◽  
Tnf Α ◽  
Factor Α

Abstract Tripartite motif-containing (TRIM) 52 (TRIM52) is a vital regulator of inflammation. However, the function and mechanisms of TRIM52 in lipopolysaccharide (LPS)-induced inflammatory injury of human periodontal ligament cells (HPDLCs) in periodontitis remain undefined. In the present research, gene expression was determined using a quantitative polymerase chain reaction and Western blot. The effect of TRIM52 on LPS-induced inflammatory injury was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and enyzme-linked immunosorbent assay (ELISA). We found that TRIM52 expression was up-regulated in LPS-treated HPDLCs. Knockdown of TRIM52 alleviated LPS-induced proliferative inhibition and apoptosis promotion in HPDLCs, as evidenced by a decrease in cleaved caspase-3 expression and caspase-3 activity. Silencing TRIM52 suppressed LPS-induced inflammatory response of HPDLCs, as indicated by the decrease in interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α) levels, and increase in IL-10 levels. TRIM52 knockdown inhibited LPS-induced activation of TLR4/nuclear factor-κ B (NF-κB) signaling pathway. Taken together, knockdown of TRIM52 mitigated LPS-induced inflammatory injury via the TLR4/NF-κB signaling pathway, providing an effective therapeutic target for periodontitis.

scholarly journals Hypoxia-regulated human periodontal ligament cells via Wnt/β-catenin signaling pathway

Medicine ◽  
2017 ◽  
Vol 96 (16) ◽  
pp. e6562 ◽  
Author(s):  
Zhili Xiao ◽  
Yineng Han ◽  
Yan Zhang ◽  
Xiaonan Zhang
Keyword(s):  
Signaling Pathway ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells

scholarly journals Cyclic compression emerged dual effects on the osteogenic and osteoclastic status of LPS-induced inflammatory human periodontal ligament cells according to loading force

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ru Jia ◽  
Yingjie Yi ◽  
Jie Liu ◽  
Dandan Pei ◽  
Bo Hu ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Osteoclast Differentiation ◽  
Cyclic Stress ◽  
Periodontal Ligament Cells ◽  
Mrna Levels ◽  
Bone Homeostasis ◽  
Periodontal Tissues ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

Abstract Background Appropriate mechanical stimulation is essential for bone homeostasis in healthy periodontal tissues. While the osteogenesis and osteoclast differentiation of inflammatory periodontal ligament cells under different dynamic loading has not been yet clear. The aim of this study is to clarify the inflammatory, osteogenic and pro-osteoclastic effects of different cyclic stress loading on the inflammatory human periodontal ligament cells (hPDLCs). Methods hPDLCs were isolated from healthy premolars and cultured in alpha minimum Eagle’s medium (α-MEM). Lipopolysaccharides (LPS) were used to induce the inflammation state of hPDLCs in vitro. Determination of LPS concentration for the model of inflammatory periodontium was based on MTT and genes expression analysis. Then the cyclic stress of 0, 0–50, 0–90 and 0–150 kPa was applied to the inflammatory hPDLCs for 5 days respectively. mRNA and protein levels of osteogenic, osteoclastic and inflammation-related markers were examined after the treatment. Results MTT and RT-PCR results showed that 10 μg/ml LPS up-regulated TNF-α, IL-1β, IL-6, IL-8 and MCP-1 mRNA levels (P < 0.05) and did not affect the cell viability (P > 0.05). The excessive loading of stress (150 kPa) with or without LPS strongly increased the expression of inflammatory-related markers TNF-α, IL-1β, IL-6, IL-8, MCP-1 (P < 0.05) and osteoclastic markers RANKL, M-CSF, PTHLH and CTSK compared with other groups (P < 0.05), but had no significant effect on osteogenic genes. While 0–90 kPa cyclic pressure could up-regulate the expression of osteogenic genes ALP, COL-1, RUNX2, OCN, OPN and OSX in the healthy hPDLSCs. Conclusions Collectively, it could be concluded that 0–150 kPa was an excessive stress loading which accelerated both inflammatory and osteoclastic effects, while 0–90 kPa may be a positive factor for the osteogenic differentiation of hPDLCs in vitro.

Genipin inhibits MMP-1 and MMP-3 release from TNF-α-stimulated human periodontal ligament cells

Biochimie ◽  
2014 ◽  
Vol 107 ◽  
pp. 391-395 ◽  
Author(s):  
Satoru Shindo ◽  
Yoshitaka Hosokawa ◽  
Ikuko Hosokawa ◽  
Kazumi Ozaki ◽  
Takashi Matsuo
Keyword(s):  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

scholarly journals Anti-inflammatory activity of psoralen in human periodontal ligament cells via estrogen receptor signaling pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Huxiao Li ◽  
Jianrong Xu ◽  
Xiaotian Li ◽  
Yi Hu ◽  
Yue Liao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Periodontal Ligament ◽  
Target Genes ◽  
Chinese Herb ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Estrogen Receptor Signaling ◽  
Receptor Signaling Pathway ◽  
Anti Inflammatory ◽  
Molecule Docking

AbstractPsoralen is one of the most effective ingredients extracted from the Chinese herb, Psoralea corylifolia L. Studies have found that psoralen has anti-inflammatory and estrogen-like effects; however, little research has been conducted to elucidate the mechanisms underlying these effects. Through the molecule docking assay, psoralen was found to have a better combination with ERα than ERβ. In human periodontal ligament cells, psoralen was found to upregulate the estrogen target genes (e.g., CTSD, PGR, TFF1) and down-regulate the expression of inflammatory cytokines (TNF-α, IL-1β, IL-6 and IL-8) stimulated by P. gingivalis LPS, as well as TLR4-IRAK4-NF-κb signaling pathway proteins. These effects were reversed by the ER antagonist ICI 182780. These results indicated that psoralen may exert anti-inflammatory effects as an agonist to ER, which could provide a theoretical basis for the use of psoralen for adjuvant therapy and prevention of periodontitis.

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