Epigenetic regulation of pro-inflammatory cytokine genes in lipopolysaccharide -stimulated peripheral blood mononuclear cells from broilers

Shen, Jing; Wu, Shengru; Guo, Wei; Liang, Saisai; Li, Xueyuan; Yang, Xiaojun

doi:10.1016/j.imbio.2016.09.009

Cited by 18 publications

(12 citation statements)

References 45 publications

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“…DNA methylation epigenetically regulates inflammatory responses by several different mechanisms. It could directly mediate the transcription of pro-inflammatory cytokines, such as IL-6, IL-8, and TNF-α, by modulating the methylation level of the gene promoters [21,37]. DNA methylation is also involved in inflammationrelated signaling pathways by epigenetically regulating the transcription of TLRs or signal transduction molecules, such as TLR2, MyD88, and TRAF6 [22,38].…”

Section: Discussionmentioning

confidence: 99%

“…DNA methylation can modulate the development of inflammation by regulating the methylation status of both pro-inflammatory cytokines and signal transduction molecules [21,22]. MyD88 and TRAF6 are two canonical transduction molecules that play central roles in activating NF-κB and MAPK signaling pathways.…”

Section: -Aza-cdr Reduced the 5mc Level Of The Traf6 Promotermentioning

confidence: 99%

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5-Aza-2’-deoxycytidine enhances lipopolysaccharide-induced inflammatory cytokine expression in human dental pulp cells by regulating TRAF6 methylation

et al. 2019

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Dental pulp inflammation is a common bacterially driven inflammation characterized by the local accumulation of inflammatory mediators in human dental pulp. DNA methylation is a crucial epigenetic modification that that plays a fundamental role in gene transcription, and its role in inflammation-related diseases has recently attracted attention. However, its role in dental pulp inflammation is poorly understood. This study is aimed to elucidate the role of DNA methylation in lipopolysaccharide (LPS)-induced inflammatory reaction in human dental pulp cells (hDPCs). hDPCs were pretreated with DNA methylation inhibitor 5-aza-2ʹ-deoxycytidine (5-Aza-CdR) and a cytokine antibody array was used to detect LPS-induced cytokine expression. The results indicated that 5-Aza-CdR significantly increased the expression of several pro-inflammatory cytokines in LPS-treated cells, including IL-6, IL-8, GM-CSF, MCP-2 and RANTES. The increased expression levels of IL-6 and IL-8 were further verified by qRT-PCR and ELISA. Furthermore, pretreatment with 5-Aza-CdR resulted in upregulation of p-IKKα/β, p-IκBα, p-p65 and p-ERK in the NK-κB and MAPK pathways. In addition, the 5mC level of the TRAF6 promoter was significantly decreased following 5-Aza-CdR pretreatment in the LPS-stimulated hDPCs. The findings indicate that 5-Aza-CdR significantly enhances the expression of proinflammatory cytokines and activates the NF-κB and MAPK signaling pathways by eliciting a decline in the 5mc level in the TRAF6 promoter in hDPCs, suggesting that DNA methylation may play an important role in dental pulp inflammation. This study highlights the important role of DNA methylation in the immunity defense of dental pulp infection.

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Section: Discussionmentioning

confidence: 99%

Section: -Aza-cdr Reduced the 5mc Level Of The Traf6 Promotermentioning

confidence: 99%

5-Aza-2’-deoxycytidine enhances lipopolysaccharide-induced inflammatory cytokine expression in human dental pulp cells by regulating TRAF6 methylation

et al. 2019

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“…Only recently have studies begun to shed light on the contribution of dnMTs to the initiation and progression of inflammatory diseases (15). A study on inflamed peripheral blood mononuclear cells (PBMCs) showed that DNMT1 expression decreased after treatment with LPS; dnMT1 modulated the methylation level of gene promoters, thus mediating the transcription of pro-inflammatory cytokines, including il-6, il-8 and tumor necrosis factor-α (TnF-α) (16). in macrophages, dnMT1 contributes to the hypermethylation of suppressor of cytokine signaling 1, a negative regulator of cytokine signal transduction, thereby enhancing the secretion of pro-inflammatory cytokines induced by LPS indirectly (17).…”

Section: Dna Methyltransferase Dnmt1 Inhibits Lipopolysaccharide-induced Inflammatory Response In Human Dental Pulp Cells Involving the Mmentioning

confidence: 99%

DNA methyltransferase DNMT1 inhibits lipopolysaccharide‑induced inflammatory response in human dental pulp cells involving the methylation changes of IL‑6 and TRAF6

Cai

Zhan

et al. 2019

Mol Med Report

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dental pulp inflammation is a pathological process characterized by local lesions in dental pulp and the accumulation of inflammatory mediators. DNA methylation of cytosine residues is a key epigenetic modification that is essential for gene transcription, and plays pivotal roles in inflammatory reactions and immune responses. However, the function of cytosine dna methylation in the innate immune defense against the inflammation of dental pulp is poorly understood. To investigate the effect of DNA methylation in inflamed dental pulp upon innate immune responses, expression levels of the dna methyltransferases (dnMT1, dnMT3a and dnMT3b) in human dental pulp cells (hdPcs) after lipopolysaccharide (LPS) stimulation were evaluated by western blotting and reverse transcription-quantitative (RT-q) PCR. Only DNMT1 expression was decreased, while the transcription of inflammatory cytokines was increased. in the immune responses of lPS-induced hdPcs, the results of RT-qPCR and ELISA showed that DNMT1 knockdown promoted the production of the pro-inflammatory cytokines, interleukin (IL)-6 and IL-8. Western blotting demonstrated that DNMT1 knockdown increased the phosphorylation levels of iKKα/β and p38 in the nF-κB and MaPK signaling pathways, respectively. Furthermore, MeDIP and RT-qPCR analysis demonstrated that the 5-methylcytosine levels of the IL-6 and TnF receptor-associated factor 6 (TRAF6) promoters were significantly decreased in DNMT1-deficient hDPCs.Taken together, these results indicated that the expression of DNMT1 was decreased after LPS stimulation in hDPCs. dnMT1 depletion increased lPS-induced cytokine secretion, and activated nF-κB and MaPK signaling; these mechanisms may involve the decreased methylation levels of the IL-6 and TRAF6 gene promoters. This study emphasized the role of DNMT1-dependent DNA methylation on the inflammation of LPS-infected dental pulp and provides a new rationale for the investigation of the molecular mechanisms of inflamed dental pulps.

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“…DNA methylation levels are influenced by heredity, age, smoking, nutritional status, and environment [29][30][31][32] and closely related to inflammatory responses, which have been the focus of many studies in recent years [33]. DNA methylation plays a regulatory role during inflammatory responses, mainly through the regulation of inflammatory cytokines [34] and inflammatory signalling pathways [35]. In addition, some inflammatory factors can promote the expression of DNMTs and increase their activity, thereby causing abnormal methylation of DNA [36].…”

Section: Discussionmentioning

confidence: 99%

Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation

Liu

Wang

et al. 2021

BMC Cardiovasc Disord

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Background ATP-binding cassette transporter A1 (ABCA1) plays a major role in high-density lipoprotein (HDL) metabolism and reverse cholesterol transport (RCT) and exerts anti-inflammatory effects. Increased ABCA1 promoter methylation level may result in the progression of coronary artery disease. Thus, the present study investigated the association between promoter methylation status of ABCA1 and inflammation in the development of premature coronary artery disease (pCAD). Methods PCAD patients and healthy individuals (n = 90 each) were recruited from the Characteristic Medical Center of the Chinese People's Armed Police Force from June to December 2019. Using pyrosequencing, the levels of ABCA1 promoter methylation in their blood samples were evaluated. Serum concentrations of lipids, interleukin 1β (IL-1β), C-reactive protein (CRP), and circulating free DNA/Neutrophil extracellular traps (cfDNA/NETs) were also routinely measured and compared between the two groups. P values < 0.05 were considered statistically significant. Results The mean ABCA1 promoter methylation levels were significantly higher in the pCAD group than in the control group (44.24% ± 3.66 vs. 36.05% ± 2.99, P < 0.001). Based on binary logistic regression analysis, ABCA1 promoter methylation level was identified as an independent risk factor for pCAD development (odds ratio = 2.878, 95% confidence interval: 1.802–4.594, P < 0.001). Furthermore, ABCA1 promoter methylation levels were negatively correlated with HDL levels (r = − 0.488, P < 0.001) and positively correlated with the levels of CRP, cfDNA/NETs, and IL-1β (r = 0.389, 0.404, 0.385, respectively; P < 0.001). Multiple regression analysis showed that the serum levels of CRP, IL-1β, and cfDNA/NETs independently affect ABCA1 promoter methylation. Conclusions Our findings indicate that high methylation levels at the ABCA1 promoter are associated with low HDL cholesterol levels and an increased risk of pCAD. Inflammatory factors and NETs may be involved in the progression of pCAD by affecting ABCA1 promoter methylation levels.

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Epigenetic regulation of pro-inflammatory cytokine genes in lipopolysaccharide -stimulated peripheral blood mononuclear cells from broilers

Cited by 18 publications

References 45 publications

5-Aza-2’-deoxycytidine enhances lipopolysaccharide-induced inflammatory cytokine expression in human dental pulp cells by regulating TRAF6 methylation

5-Aza-2’-deoxycytidine enhances lipopolysaccharide-induced inflammatory cytokine expression in human dental pulp cells by regulating TRAF6 methylation

DNA methyltransferase DNMT1 inhibits lipopolysaccharide‑induced inflammatory response in human dental pulp cells involving the methylation changes of IL‑6 and TRAF6

Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation

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