<i>Porphyromonas gingivalis</i> lipopolysaccharide regulates ephrin/Eph signalling in human periodontal ligament fibroblasts

Li, M.; Zhang, C.; Jin, Lijian; Matsuo, Koichi; Yang, Yanqi

doi:10.1111/jre.12463

Cited by 7 publications

(5 citation statements)

References 44 publications

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“…Our data showed that the RANKL/OPG ratio was higher under co-stimulation by CF and LPS than under mechanical stimulation alone, consistent with the results of other studies (Nokhbehsaim et al, 2010;Romer et al, 2013;Yamamoto et al, 2011). In our earlier research (Li et al, 2017), we observed upregulated ephrinA2 and downregulated EphB4 expression in PDLCs treated with LPS, suggestive of the inflammation-related dysfunction of bone remodeling via ephrinA2 and EphB4 signaling.…”

Section: Effects Of Ephrina2 Knockdown On Pdlcs Under Simultaneous Lp...supporting

confidence: 92%

Lipopolysaccharides affect compressed periodontal ligament cells via Eph–ephrin signaling

Tang

Zhang

et al. 2021

Oral Diseases

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Objectives The aim of this study is to investigate the underlying mechanism of the recovery of periodontal ligament cells (PDLCs) sequentially exposed to inflammation and mechanical loading. Materials and Methods We divided PDLCs into four groups: control; compressive force (CF) alone (2.0 g/cm2); lipopolysaccharides (LPS) pretreatment (0.1 μg/ml) followed by simultaneous LPS and CF stimulation, simulating uncontrolled periodontitis; and LPS pretreatment followed by CF exposure, simulating controlled periodontitis. The expression of EphB4‐ephrinB2 and EphA2‐ephrinA2, and the level of osteoclastogenesis and osteogenesis were evaluated. Results Simultaneous stimulation by LPS and CF, compared with CF alone and sequential LPS and CF exposure, significantly suppressed EphB4 and enhanced ephrinA2 expression. Similarly, the most intense osteoclastic differentiation was observed under simultaneous LPS and CF stimulation, while sequential exposure to LPS and CF only slightly increased osteoclastic cell numbers. Both the activation of EphB4 signaling and ephrinA2 silencing lowered osteoclastic differentiation, which had previously been upregulated by simultaneous LPS and CF stimulation. These treatments also increased osteogenic differentiation. Conclusions Simultaneous LPS and CF stimulation critically enhances osteoclastogenesis in PDLCs through the suppression of EphB4 and the induction of ephrinA2 signaling. Sequential LPS and CF exposure partially abolishes the osteolytic effects of simultaneous stimulation.

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Section: Effects Of Ephrina2 Knockdown On Pdlcs Under Simultaneous Lp...supporting

confidence: 92%

Lipopolysaccharides affect compressed periodontal ligament cells via Eph–ephrin signaling

Tang

Zhang

et al. 2021

Oral Diseases

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“…Even though, Li et al studied the effect of P. gingivalis - LPS on Eph/Ephrin signals and found that the inhibition of EphB4 expression had no significant impact on EphrinB2 in periodontal ligament fibroblasts . Zhao et al proposed that in bone metabolism, the EphB4 receptor on osteoblasts activated the EphrinB2 ligand on osteoclasts to inhibit osteoclasts, while EphrinB2 activated the EphB4 receptor to promote osteogenesis, which played a significant role in the bidirectional signaling .…”

Section: Discussionmentioning

confidence: 99%

“…31 Even though, Li et al studied the effect of P. gingivalis-LPS on Eph/Ephrin signals and found that the inhibition of EphB4 expression had no significant impact on EphrinB2 in periodontal ligament fibroblasts. 32 Zhao et al…”

Section: ■ Discussionmentioning

confidence: 99%

Imbalanced EphB4/EphrinB2 Signaling Modulates Bone Resorption in Periodontitis Induced by Porphyromonas gingivalis

Fu,

Zhang,

Liu

et al. 2024

ACS Infect. Dis.

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Periodontitis, a chronic infectious disease in periodontal tissues, is characterized by an imbalance of alveolar bone resorption and remodeling, which eventually results in tooth loosening and even tooth loss. The etiology of periodontitis is polymicrobial synergy and dysbiosis, in which Porphyromonas gingivalis (P. gingivalis) is one of the primary pathogens responsible for periodontitis progression. The interplay of EphrinB2/EphB4 is crucial for osteoblast−osteoclast communication during bone remodeling and healing. This study investigates the mechanism of EphB4/EphrinB2 transduction modulating osteogenesis inhibition and bone resorption in periodontitis induced by P. gingivalis. An in vivo model of chronic periodontitis provoked by P. gingivalis was constructed, the inflammation and bone resorption were evaluated. The expression of EphB4 and EphrinB2 proteins in periodontal tissues was detected, which was also evaluated, respectively, in osteoblasts and osteoclasts infected with P. gingivalis in vitro. Then, a simulated coculture model of osteoblasts and osteoclasts was established to activate the forward and reverse pathways of EphB4/EphrinB2 with P. gingivalis infection. This study showed that P. gingivalis infection promoted alveolar bone resorption in rats and enhanced EphB4 and EphrinB2 expression in periodontal tissues. EphB4 and molecules associated with osteogenesis in osteoblasts infected with P. gingivalis were inhibited, while EphrinB2 and osteoclast differentiation-related markers in osteoclasts were activated. In conclusion, this study suggested that EphB4/EphrinB2 proteins were involved in alveolar bone remodeling in the process of periodontitis induced by P. gingivalis infection. Moreover, attenuated EphB4/EphrinB2 with P. gingivalis infection weakened osteoblast activity and enhanced osteoclast activity.

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“…Low concentrations of LPS promote the proliferation of HPDLF. One direct approach may be that LPS promotes intracellular gene expression in cells by activating signaling pathways, such as ephrin/Eph [ 41 ], or that LPS affects Ca 2+ the transmembrane transport inside and outside cells [ 42 ]; another indirect approach is that LPS promotes cell proliferation by stimulating the production of bioactive factors in cells. However, with increased LPS intervention times, cell tolerance decreases, cells overmature, production capacity decreases, and the secretion of multiple enzymes, such as matrix metalloproteinases, increases, leading to cytotoxicity [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Metformin Improves Burn Wound Healing by Modulating Microenvironmental Fibroblasts and Macrophages

Shi

Jiang

et al. 2022

Cells

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Metformin, a biguanide, exerts different functions through various signaling pathways. In order to investigate the function and mechanism of metformin in burn wounds, we established burn rat models, subcutaneously injected metformin to treat the wounds, and observed the morphologies and the expression of collagen I, collagen III, fibronectin, and pro-inflammatory markers. In vitro experiments were performed to investigate the effects of metformin on the proliferation, migration, and collagen I synthesis of the mouse embryonic fibroblast (NIH 3T3) cell line and on the proliferation, apoptosis, and immune response of the mouse mononuclear macrophage (RAW 264.7) cell line. Finally, we studied the regulatory effects of metformin on a co-culture of RAW 264.7/NIH 3T3 cells. We found that 100 mM of metformin reduced dermal thickness, collagen I deposition, and mRNA expression of IL1β and CCL2 in rat burn wounds. In vitro experiments revealed that metformin inhibited the proliferation of NIH 3T3 and RAW 264.7 cells. Metformin attenuated NIH 3T3 cell migration via the AMPK/mTOR pathway and attenuated collagen I synthesis through the TGFβ1/Smad3 pathway. Metformin inhibited the apoptosis of RAW 264.7 cells induced by 10 μg/mL LPS. Metformin downregulated the mRNA expression of IL1β and CCL2 in RAW 264.7 cells under 1 μg/mL LPS induction by inhibiting NF-κB p65 phosphorylation. In a RAW 264.7/NIH 3T3 co-culture, metformin attenuated collagen I synthesis in NIH 3T3 cells by inhibiting RAW 264.7 paracrine secretion of TGF-β1. This provides new evidence related to the development of metformin for potentially improving burn wound healing.

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Porphyromonas gingivalis lipopolysaccharide regulates ephrin/Eph signalling in human periodontal ligament fibroblasts

Cited by 7 publications

References 44 publications

Lipopolysaccharides affect compressed periodontal ligament cells via Eph–ephrin signaling

Lipopolysaccharides affect compressed periodontal ligament cells via Eph–ephrin signaling

Imbalanced EphB4/EphrinB2 Signaling Modulates Bone Resorption in Periodontitis Induced by Porphyromonas gingivalis

Metformin Improves Burn Wound Healing by Modulating Microenvironmental Fibroblasts and Macrophages

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