<i>Enterococcus faecalis</i> OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Li, Yang; Wen, Cheng; Zhong, Jialin; Ling, Junqi; Jiang, Qianzhou

doi:10.1111/odi.13996

Cited by 7 publications

(12 citation statements)

References 60 publications

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“…In the present study, E. faecalis infection increased the number of TUNEL-positive cells and apoptotic cells in the early and late phases, which was also observed in our previous study on MC3T3-E1 and MG63 cells infected with E. faecalis [10,12]. We also noticed that necrotic cells of which the cell membrane integrity is damaged may also be stained as Annexin V-FITC/PI double-positive, as previous studies reported [29,30].…”

Section: Discussionsupporting

confidence: 91%

“…Hence, it is crucial to examine the role of E. faecalis on osteoblast apoptosis in PAP. Our previous study found that E. faecalis strains from the root canals of teeth with PAP trigger apoptosis in mouse MC3TE-E1 and human MG63 cell lines [10,12]. However, the effect of E. faecalis on apoptosis in human primary osteoblasts and its mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…To examine the effect of E. faecalis OG1RF on osteoblast apoptosis, the cells were plated onto 24-well plates at 1.5 × 10 5 /well or six-well plates at 6 × 10 5 /well. At the indicated infection time points, E. faecalis OG1RF at the corresponding multiplicity of infection (MOI) was added to the osteoblast culture, as previously described [12].…”

Section: Cultures Of Osteoblasts and E Faecalis Og1rfmentioning

confidence: 99%

“…The infected cells were incubated with 0.5 mL of JC-1 staining solution (#C2006; Beyotime, Shanghai, China) and evaluated using a FACS-Calibur flow cytometer. The ΔΨm was estimated by calculating the ratio of red/green fluorescence intensities as previously reported [12].…”

Section: Flow Cytometrymentioning

confidence: 99%

“…The detection of E. faecalis in infected root canals has been associated with the occurrence of periapical lesions larger than 3 mm, indicating the role of E. faecalis in PAP and endodontic treatment failure [9]. Recent studies have found that E. faecalis induces apoptosis in mouse osteoblast-like MC3T3 cells and human osteosarcoma MG63 cells [10][11][12]. However, there may be a difference between the effect of E. faecalis infection in primary osteoblasts and osteoblast-like cells from different origins [10,13].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Enterococcus faecalis OG1RF on human calvarial osteoblast apoptosis

Sun

Wen

et al. 2022

BMC Oral Health

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Background Enterococcus faecalis is a dominant pathogen in the root canals of teeth with persistent apical periodontitis (PAP), and osteoblast apoptosis contributes to imbalanced bone remodelling in PAP. Here, we investigated the effect of E. faecalis OG1RF on apoptosis in primary human calvarial osteoblasts. Specifically, the expression of apoptosis-related genes and the role of anti-apoptotic and pro-apoptotic members of the BCL-2 family were examined. Methods Primary human calvarial osteoblasts were incubated with E. faecalis OG1RF at multiplicities of infection corresponding to infection time points. Flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay, caspase-3/-8/-9 activity assay, polymerase chain reaction (PCR) array, and quantitative real-time PCR were used to assess osteoblast apoptosis. Results E. faecalis infection increased the number of early- and late-phase apoptotic cells and TUNEL-positive cells, decreased the mitochondrial membrane potential (ΔΨm), and activated the caspase-3/-8/-9 pathway. Moreover, of all 84 apoptosis-related genes in the PCR array, the expression of 16 genes was upregulated and that of four genes was downregulated in the infected osteoblasts. Notably, the mRNA expression of anti-apoptotic BCL2 was downregulated, whereas that of the pro-apoptotic BCL2L11, HRK, BIK, BMF, NOXA, and BECN1 and anti-apoptotic BCL2A1 was upregulated. Conclusions E. faecalis OG1RF infection triggered apoptosis in human calvarial osteoblasts, and BCL-2 family members acted as regulators of osteoblast apoptosis. Therefore, BCL-2 family members may act as potential therapeutic targets for persistent apical periodontitis.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Cultures Of Osteoblasts and E Faecalis Og1rfmentioning

confidence: 99%

Section: Flow Cytometrymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Enterococcus faecalis OG1RF on human calvarial osteoblast apoptosis

Sun

Wen

et al. 2022

BMC Oral Health

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Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Liu

Fan

2023

Journal Cellular Physiology

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Programmed cell death (PCD) has been a research focus for decades and different mechanisms of cell death, such as necroptosis, pyroptosis, ferroptosis, and cuproptosis have been discovered. Necroptosis, a form of inflammatory PCD, has gained increasing attention in recent years due to its critical role in disease progression and development. Unlike apoptosis, which is mediated by caspases and characterized by cell shrinkage and membrane blebbing, necroptosis is mediated by mixed lineage kinase domain‐like protein (MLKL) and characterized by cell enlargement and plasma membrane rupture. Necroptosis can be triggered by bacterial infection, which on the one hand represents a host defense mechanism against the infection, but on the other hand can facilitate bacterial escape and worsen inflammation. Despite its importance in various diseases, a comprehensive review on the involvement and roles of necroptosis in apical periodontitis is still lacking. In this review, we tried to provide an overview of recent progresses in necroptosis research, summarized the pathways involved in apical periodontitis (AP) activation, and discussed how bacterial pathogens induce and regulated necroptosis and how necroptosis would inhibit bacteria. Furthermore, the interplay between various types of cell death in AP and the potential treatment strategy for AP by targeting necroptosis were also discussed.

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Programmed cell death of periodontal ligament cells

He,

Fu,

Yao

et al. 2023

Journal Cellular Physiology

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The periodontal ligament is a crucial tissue that provides support to the periodontium. Situated between the alveolar bone and the tooth root, it consists primarily of fibroblasts, cementoblasts, osteoblasts, osteoclasts, periodontal ligament stem cells (PDLSCs), and epithelial cell rests of Malassez. Fibroblasts, cementoblasts, osteoblasts, and osteoclasts are functionally differentiated cells, whereas PDLSCs are undifferentiated mesenchymal stem cells. The dynamic development of these cells is intricately linked to periodontal changes and homeostasis. Notably, the regulation of programmed cell death facilitates the clearance of necrotic tissue and plays a pivotal role in immune response. However, it also potentially contributes to the loss of periodontal supporting tissues and root resorption. These findings have significant implications for understanding the occurrence and progression of periodontitis, as well as the mechanisms underlying orthodontic root resorption. Further, the regulation of periodontal ligament cell (PDLC) death is influenced by both systemic and local factors. This comprehensive review focuses on recent studies reporting the mechanisms of PDLC death and related factors.

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Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Cited by 7 publications

References 60 publications

Effect of Enterococcus faecalis OG1RF on human calvarial osteoblast apoptosis

Effect of Enterococcus faecalis OG1RF on human calvarial osteoblast apoptosis

Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Programmed cell death of periodontal ligament cells

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