Advanced glycation end products (AGEs) and their receptor (RAGE) induce apoptosis of periodontal ligament fibroblasts

Li, D.X.; Deng, Tianzheng; Lv, Jing; Ke, Jie

doi:10.1590/1414-431x20143996

Cited by 38 publications

(29 citation statements)

References 37 publications

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“…When the adherent cells reached 80% confluence, the cells were treated with 100 μg/mL AGEs for 6, 8, or 24 hours to investigate the influence of AGEs on HPDLCs, respectively. The optimal concentration of AGEs was chosen based on preliminary dose‐response studies of 10‐200 μg/mL . After AGEs pre‐incubation, 10 μg/mL MDP was added and incubated for 24 hours.…”

Section: Methodsmentioning

confidence: 99%

The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

Zhang

et al. 2019

J of Periodontal Research

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Background and Objective Diabetes influences the frequency and development of periodontitis. Inflammation of human periodontal ligament cells (HPDLCs) participates in this pathologic process. Hence, this study aims to explore whether advanced glycation end products (AGEs), by‐products of diabetes, could exaggerate inflammation induced by muramyl dipeptide (MDP) in HPDLCs, and whether nucleotide‐binding oligomerization domain‐like receptors (NLRs) signaling pathway was involved. Material and Methods Human periodontal ligament cells were pre‐treated with 100 μg/mL AGEs for 24 hours and stimulated with 10 μg/mL MDP for 24 hours. IL‐6, IL‐1β, and RAGE were detected, and the activation of NF‐κB signaling pathway was observed. The expression of NLRs was evaluated with or without silencing RAGE or blocking NF‐κB pathway under AGEs stimulation. Statistical analyses were performed by using independent sample t test. Results Advanced glycation end products induced significant increase of inflammatory cytokines in HPDLCs (P < 0.05). Results of western blot (WB) showed that after 45 minutes stimulation of AGEs, p‐p65/p65 ratio peaked; AGEs promoted the expression of NLRP1, NLRP3, and apoptosis‐associated speck‐like protein containing a CARD (ASC). After silencing RAGE or blocking NF‐κB pathway, the up‐regulation of NLRs protein caused by AGEs was attenuated. Additionally, AGEs pre‐treatment could enhance the inflammatory response of MDP and the expression of NLRs, which were demonstrated by more expression of IL‐6, IL‐1β, NOD2, NLRP1, NLRP3, and ASC. Conclusion Advanced glycation end products induced inflammatory response in HPDLCs via NLRP1‐inflammasome and NLRP3‐inflammasome activation in which NF‐κB signal pathway was involved. Besides, AGEs promoted the inflammatory response of MDP via NOD2, NLRP1‐inflammasome, and NLRP3‐inflammasome.

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Section: Methodsmentioning

confidence: 99%

The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

Zhang

et al. 2019

J of Periodontal Research

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“…In the study of the photoaging mechanism, it was previously demonstrated that UV radiation may lead to the apoptosis of a large number of dermal fibroblasts (light damage), and apoptosis promoted the development of photoaging (9,31). Hoechst staining and flow cytometry methods were utilized in the present study to determine whether UVA radiation was able to induce fibroblast apoptosis, which was more obvious at higher radiation doses.…”

Section: Discussionmentioning

confidence: 99%

GSK126 (EZH2 inhibitor) interferes with ultraviolet A radiation‑induced photoaging of human skin fibroblast cells

2018

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Abstract. Polycomb group genes (PcG) encode chromatin modification proteins that are involved in the epigenetic regulation of cell differentiation, proliferation and the aging processes. The key subunit of the PcG complex, enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2), has a central role in a variety of mechanisms, such as the formation of chromatin structure, gene expression regulation and DNA damage. In the present study, ultraviolet A (UVA) was used to radiate human dermal fibroblasts in order to construct a photo-aged cell model. Subsequently, the cell viability assay, Hoechst staining, apoptosis detection using flow cytometry, senescence-associated β-galactosidase (SA-β-gal) staining and erythrocyte exclusion experiments were performed. GSK126, a histone methylation enzyme inhibitor of EZH2, was used as an experimental factor. Results suggested that GSK126 downregulated the mRNA expression levels of EZH2 and upregulated the mRNA expression levels of BMI-1. Notably, GSK126 affected the transcription of various photoaging-related genes and thus protected against photoaging induced by UVA radiation.

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“…Recently, it has been reported that AGEs bind to its receptor in periodontal ligament fibroblasts provoking apoptosis and inhibition of collagen production (Li et al . ). Therefore, AGEs could impair periapical repair after RCT.…”

Section: Association Between Endodontics and Diabetes Mellitusmentioning

confidence: 97%

Endodontic medicine: connections between apical periodontitis and systemic diseases

2015

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The prevalence of apical periodontitis (AP) in Europe has been reported to affect 61% of individuals and 14% of teeth, and increase with age. Likewise, the prevalence of root canal treatment (RCT) in Europe is estimated to be around 30-50% of individuals and 2-9% of teeth with radiographic evidence of chronic persistent AP in 30-65% of root filled teeth (RFT). AP is not only a local phenomenon and for some time the medical and dental scientific community have analysed the possible connection between apical periodontits and systemic health. Endodontic medicine has developed, with increasing numbers of reports describing the association between periapical inflammation and systemic diseases. The results of studies carried out both in animal models and humans are not conclusive, but suggest an association between endodontic variables, that is AP and RCT, and diabetes mellitus (DM), tobacco smoking, coronary heart disease and other systemic diseases. Several studies have reported a higher prevalence of periapical lesions, delayed periapical repair, greater size of osteolityc lesions, greater likelihood of asymptomatic infections and poorer prognosis for RFT in diabetic patients. On the other hand, recent studies have found that a poorer periapical status correlates with higher HbA1c levels and poor glycaemic control in type 2 diabetic patients. However, there is no scientific evidence supporting a causal effect of periapical inflammation on diabetes metabolic control. The possible association between smoking habits and endodontic infection has also been investigated, with controversial results. The aim of this paper was to review the literature on the association between endodontic variables and systemic health (especially DM and smoking habits).

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Advanced glycation end products (AGEs) and their receptor (RAGE) induce apoptosis of periodontal ligament fibroblasts

Cited by 38 publications

References 37 publications

The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

GSK126 (EZH2 inhibitor) interferes with ultraviolet A radiation‑induced photoaging of human skin fibroblast cells

Endodontic medicine: connections between apical periodontitis and systemic diseases

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