Epigenetic characteristics in inflammatory candidate genes in aggressive periodontitis

Schulz, Susanne; Immel, Uta Dorothee; Just, Louise; Schaller, Hans‐Günter; Gläser, Christiane; Reichert, Stefan

doi:10.1016/j.humimm.2015.10.007

Cited by 48 publications

(56 citation statements)

References 34 publications

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“…The present study extends pioneering research on epigenetics in periodontal research that has investigated methylation changes in the promoter regions of disease-relevant genes coding for extracellular matrix proteins [27], chemokines and cytokines [28][29][30], and signaling molecules [31,32]. The importance of this research is underscored by recent reviews on epigenetics in periodontal disease [33,34].…”

Section: Introductionmentioning

confidence: 61%

Inhibitors of DNA methylation support TGF-β1-induced IL11 expression in gingival fibroblasts

Șufaru

Beikircher

Weinhäusel

et al. 2017

J Periodontal Implant Sci

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Purpose: Oral wound healing requires gingival fibroblasts to respond to local growth factors. Epigenetic silencing through DNA methylation can potentially decrease the responsiveness of gingival fibroblasts to local growth factors. In this study, our aim was to determine whether the inhibition of DNA methylation sensitized gingival fibroblasts to transforming growth factor-β1 (TGF-β1). Methods: Gingival fibroblasts were exposed to 5-aza-2'-deoxycytidine (5-aza), a clinically approved demethylating agent, before stimulation with TGF-β1. Gene expression changes were evaluated using quantitative polymerase chain reaction (PCR) analysis. DNA methylation was detected by methylation-sensitive restriction enzymes and PCR amplification. Results: We found that 5-aza enhanced TGF-β1-induced interleukin-11 (IL11) expression in gingival fibroblasts 2.37-fold (P=0.008). 5-aza had no significant effects on the expression of proteoglycan 4 (PRG4) and NADPH oxidase 4 (NOX4). Consistent with this, 5-aza caused demethylation of the IL11 gene commonly next to a guanosine (CpG) island in gingival fibroblasts. The TGF-β type I receptor kinase inhibitor SB431542 impeded the changes in IL11 expression, indicating that the effects of 5-aza require TGF-β signaling. 5-aza moderately increased the expression of TGF-β type II receptor (1.40-fold; P=0.009), possibly enhancing the responsiveness of fibroblasts to TGF-β1. As part of the feedback response, 5-aza increased the expression of the DNA methyltransferases 1 (DNMT1) (P=0.005) and DNMT3B (P=0.002), which are enzymes responsible for gene methylation. Conclusions: These in vitro data suggest that the inhibition of DNA methylation by 5-aza supports TGF-β-induced IL11 expression in gingival fibroblasts.

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Section: Introductionmentioning

confidence: 61%

Inhibitors of DNA methylation support TGF-β1-induced IL11 expression in gingival fibroblasts

Șufaru

Beikircher

Weinhäusel

et al. 2017

J Periodontal Implant Sci

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“…Baseline blood samples were obtained and patients reported their number of teeth according to the following tooth loss levels: "26-32 (All)" [lowest level], [20][21][22][23][24][25][15][16][17][18][19][1][2][3][4][5][6][7][8][9][10][11][12][13][14]and "No Teeth" [highest level]. Linear and Cox regression models assessed associations between tooth loss levels, biomarker levels and the relationship between tooth loss levels and outcomes, respectively.…”

Section: Methods and Resultsmentioning

confidence: 99%

“…However, our findings could represent a challenge to the inflammation hypothesis as the highest levels of inflammatory markers were observed among the edentulous, who are most likely rid of oral substrates for inflammation. This could indicate that intrinsic factors and not PD explain the inflammatory activity, for instance proinflammatory genetic traits and epigenetic modifications common to both advanced PD and CHD [23,24]. However, it is also conceivable that many years' exposure to chronic oral inflammation could instigate a secondary response in other locations, e.g .…”

Section: Discussionmentioning

confidence: 99%

Associations between tooth loss and prognostic biomarkers and the risk for cardiovascular events in patients with stable coronary heart disease

Vedin

Hagström

Östlund

et al. 2017

International Journal of Cardiology

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“…This finding suggests a potential application of trichostatin A for bone regeneration therapy by hPDL cells. [86] …”

Section: Osteogenic Differentiation Of Human Periodontal Ligament (Hpmentioning

confidence: 99%

“…[86] Epigenetic modifications also affect the immune response. In gingival biopsies taken from patients with AgP, CpG methylation of CCL25 (1.73% vs. 2.59%, P = 0.015) and IL17C (6.89% vs. 19.27%, P = 0.002) was significantly reduced as compared with periodontally healthy tissues.…”

Section: Epigenetics In Immune Responsementioning

confidence: 99%

Untitled

Juneius

2016

AJP

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Aim: To review the literature on the oral health status of the population, evidence-based understanding of epigenetic mechanisms, and its significant role in diseases occurring in the oral cavity. Background: Epigenetics is the study of heritable changes in gene expression that does not involve changes to the underlying DNA sequence. In other words, it is a change in phenotype without a change in genotype, which in turn affects the way cells read genes. Epigenetic change is a regular and natural occurrence but can also be influenced by several factors including age, the environment/lifestyle, and disease state. The field of epigenetics is quickly growing, and it is believed that both the environment and lifestyle can interact with the genome to influence epigenetic change. These changes may be reflected at various stages throughout a person's life and even in later generations. Conclusion: Epigenetic codes help us understand the biological phenotype that arises from the interaction of the human genome with the environment in health and in disease. Epigenetics is a major turn away from molecular biology. Current epigenetics not only offers new insights into gene regulation and heredity, but also it challenges the way we think about evolution, genetics, and development. Most interestingly, it suggests testable mechanisms whereby environmental factors (ranging from stress to infection) can influence genetic expression.

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Epigenetic characteristics in inflammatory candidate genes in aggressive periodontitis

Cited by 48 publications

References 34 publications

Inhibitors of DNA methylation support TGF-β1-induced IL11 expression in gingival fibroblasts

Inhibitors of DNA methylation support TGF-β1-induced IL11 expression in gingival fibroblasts

Associations between tooth loss and prognostic biomarkers and the risk for cardiovascular events in patients with stable coronary heart disease

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