DNA甲基化
甲基化
表观遗传学
发起人
牙周炎
基因表达
实时聚合酶链反应
分子生物学
生物
白细胞介素6
男科
聚合酶链反应
基因
内科学
内分泌学
医学
免疫学
遗传学
细胞因子
作者
Caroline Sousa Ribeiro Adeodato,Sheila Coelho Soares-Lima,Paula Vieira Batista,Marina Chianello Nicolau Fagundes,Diego Camuzi,Sandro Junio Oliveira Tavares,Luis Felipe Ribeiro Pinto,Miriam Zaccaro Scelza
标识
DOI:10.1016/j.archoralbio.2023.105694
摘要
Apical periodontitis is a periradicular tissue disorder that usually arises from infection by microorganisms in the root canal system resulting in local bone resorption. This usually involves the dysregulation of inflammatory mediators, which can be mediated by epigenetic mechanisms. Thus, the objective of this study was to evaluate Interleukin 6 (IL6) and Interleukin 1β (IL1β) and DNA methylation and gene expression levels in apical periodontitis. Gene expression was analyzed in 60 participants using quantitative polymerase chain reaction, while the methylation levels of IL6 and IL1β promoters were analyzed in 72 patients using pyrosequencing. All statistical analyzes were performed using the GraphPad Prism software version 8.0. The p value was considered statistically significant when < 0.05. A significantly higher IL6 and IL1β expression levels were observed in cases relative to controls (fold-changes of 27.4 and 11.43, respectively, and p < 0.0001). By comparing the same groups, lower promoter methylation levels were observed for both genes in cases (methylation percentage delta relative to controls of −24.57% and −16.02%, respectively, and p < 0.0001). A significant inverse correlation between gene expression and promoter methylation was observed for both IL6 (p = 0.0002) and IL1β (p = 0.001). Neither IL6 expression nor promoter methylation were significantly associated with cases’ age, smoking history, alcohol consumption history or sex. For IL1β, alcoholic cases showed lower methylation level relative to non-alcoholic cases (p = 0.01), while females showed higher methylation levels relative to males (p = 0.03). Our data suggest a role for DNA methylation in IL6 and IL1β upregulation in apical periodontitis.
科研通智能强力驱动
Strongly Powered by AbleSci AI