Up-regulated ferritin in periodontitis promotes inflammatory cytokine expression in human periodontal ligament cells through transferrin receptor via ERK/P38 MAPK pathways

2019 ◽  
Vol 133 (1) ◽  
pp. 135-148 ◽  
Author(s):  
Wenxue Huang ◽  
Yalin Zhan ◽  
Yunfei Zheng ◽  
Ye Han ◽  
Wenjie Hu ◽  
...  
Keyword(s):  
Transferrin Receptor ◽  
Intracellular Signaling ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Dependent Manner ◽  
Inflammatory Infiltration ◽  
Intracellular Signaling Pathway ◽  
Periodontal Tissues ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

Abstract Objective: Ferritin, an iron-binding protein, is ubiquitous and highly conserved; it plays a crucial role in inflammation, which is the main symptom of periodontitis. Full-length cDNA library analyses have demonstrated abundant expression of ferritin in human periodontal ligament. The aims of the present study were to explore how ferritin is regulated by local inflammation, and to investigate its functions and mechanisms of action in the process of periodontitis. Methods: Human gingival tissues were collected from periodontitis patients and healthy individuals. Experimental periodontitis was induced by ligature of second molars in mice. The expression of ferritin light polypeptide (FTL) and ferritin heavy polypeptide (FTH) were assessed by immunohistochemistry. Meanwhile, after stimulating human periodontal ligament cells (HPDLCs) with P. gingivalis-lipopolysaccharide (LPS), interleukin (IL)-6, and tumor necrosis factor-α (TNF-α), the expression of FTH and FTL were measured. Then, IL-6 and IL-8 were measured after incubation with different concentrations of apoferritin (iron-free ferritin) and several intracellular signaling pathway inhibitors, or after knockdown of the transferrin receptor. Results: Both FTH and FTL were substantially higher in inflamed periodontal tissues than in healthy tissues. The location of the elevated expression correlated well with the extent of inflammatory infiltration. Moreover, expression of FTH and FTL were enhanced after stimulation with P. gingivalis-LPS, IL-6, TNF-α. Apoferritin induced the production of IL-6 and IL-8 in a dose-dependent manner partly through binding to the transferrin receptor and activating ERK/P38 signaling pathways in HPDLCs. Conclusions: Ferritin is up-regulated by inflammation and exhibits cytokine-like activity in HPDLCs inducing a signaling cascade that promotes expression of pro-inflammatory cytokines associated with periodontitis.

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.

scholarly journals Cyclic compression emerged dual effects on the bone homeostasis of LPS-induced inflammatory human periodontal ligament cells according to loading force

2019 ◽  
Author(s):  
Ru Jia ◽  
Yingjie Yi ◽  
Jie Liu ◽  
Dandan Pei ◽  
Bo Hu ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Cyclic Stress ◽  
Periodontal Ligament Cells ◽  
Mrna Levels ◽  
Bone Homeostasis ◽  
Protein Levels ◽  
Periodontal Tissues ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

Abstract Background: Appropriate mechanical stimulation is essential for bone homeostasis in healthy periodontal tissues. While the bone homeostasis of inflammatory periodontal tissues 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, 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 and RUNX2 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 bone homeostasis of hPDLCs in vitro

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

2019 ◽  
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

Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-α- and dexamethasone-stimulated human periodontal ligament cells

Cytokine ◽  
2006 ◽  
Vol 35 (1-2) ◽  
pp. 67-76 ◽  
Author(s):  
Hwa-Jeong Lee ◽  
Jin-Woo Cho ◽  
Sang-Cheol Kim ◽  
Kyung-Hwa Kang ◽  
Sun-Kyung Lee ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Map Kinases ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

Effects of HSP70 on the compression force-induced TNF-α and RANKL expression in human periodontal ligament cells

2010 ◽  
Vol 60 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Masami Mitsuhashi ◽  
Masaru Yamaguchi ◽  
Tadashi Kojima ◽  
Ryo Nakajima ◽  
Kazutaka Kasai
Keyword(s):  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Compression Force ◽  
Rankl Expression ◽  
Human Periodontal Ligament Cells ◽  
Tnf Α

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.

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