Department of Periodontology, Tufts University School of Dental Medicine, Boston, MA, USA.
Department of Periodontology, Guarulhos Univerity, São Paulo, Brazil.
Evid Based Dent. 2023 Dec;24(4):168-169. doi: 10.1038/s41432-023-00939-8. Epub 2023 Oct 9.
The research used an in vitro cell exposure model and multi-omics integration of transcriptome and epigenome profiling to compare the molecular effects of e-cigarettes and tobacco smoke on dental stem cells.
The study aimed to compare the effects of e-cigarette and tobacco smoke on periodontal stem cells using a multi-omics approach to understand gene regulation.
This research studied primary human gingival mesenchymal stem cells (GMSCs) and periodontal ligament stem cells (PDLSCs) obtained from healthy donors. The cells were subjected to tobacco smoke, e-cigarette aerosol (both tobacco and menthol flavors), e-cigarette liquid (both tobacco and menthol flavors), or untreated conditions using an in vitro exposure system. RNA sequencing and bioinformatics analysis were used to profile the transcriptome and identify differential gene expression. Additionally, chromatin immunoprecipitation sequencing (ChIP-seq) was used to conduct genome-wide histone modification mapping for H3K27me3. Transcriptome profiling was combined with histone modification characterization to understand gene regulatory mechanisms. The study compared the effects of smoke versus e-cigarette, aerosol versus liquid exposure, and tobacco versus menthol flavor on gene expression and epigenetic landscapes in the two oral stem cell populations.
The use of tobacco smoke caused damage to the DNA and nucleus in GMSCs, as well as mitochondrial dysfunction in PDLSCs. Regarding e-cigarettes, the aerosol and liquid affected non-coding RNA expression differently. The chemokine CXCL2 was found to be downregulated by aerosol but upregulated by liquid in GMSCs. An integrative analysis revealed that the upregulation of CXCL2 caused by e-liquid involved reduced H3K27me3 and activation of distal enhancers. On the other hand, aerosol exposure maintained H3K27me3 levels, while direct e-liquid exposure resulted in genome-wide reductions in H3K27me3, particularly in enhancer regions. Overall, the specific delivery methods and components of e-cigarettes caused unique changes in the transcriptome and epigenome of oral stem cells.
E-cigarettes affect oral stem cells differently than tobacco smoke. Their aerosol and liquid have varying impacts on gene expression and regulatory landscapes in oral cells. Multi-omics approaches are important to understanding the molecular changes caused by e-cigarette components. This can help with toxicological assessments and determine their impact on periodontal health. Transcriptome and epigenome profiling are powerful tools to examine the unique molecular mechanisms involved in cellular responses to e-cigarettes.
本研究采用体外细胞暴露模型和转录组和表观基因组谱的多组学整合，比较电子烟和烟草烟雾对牙源性干细胞的分子影响。
本研究旨在通过多组学方法比较电子烟和烟草烟雾对牙周干细胞的影响，以了解基因调控。
本研究使用来自健康供体的原代人牙龈间充质干细胞（GMSCs）和牙周韧带干细胞（PDLSCs）。使用体外暴露系统，将细胞暴露于烟草烟雾、电子烟气溶胶（含烟草和薄荷味）、电子烟液（含烟草和薄荷味）或未处理条件下。使用 RNA 测序和生物信息学分析对转录组进行分析，以鉴定差异表达基因。此外，还使用染色质免疫沉淀测序（ChIP-seq）进行全基因组组蛋白修饰 H3K27me3 图谱绘制。将转录组谱分析与组蛋白修饰特征相结合，以了解基因调控机制。本研究比较了烟雾与电子烟、气溶胶与液体暴露以及烟草与薄荷味对两种口腔干细胞群体中基因表达和表观遗传景观的影响。
烟草烟雾的使用导致 GMSCs 的 DNA 和核损伤以及 PDLSCs 的线粒体功能障碍。关于电子烟，气溶胶和液体对非编码 RNA 表达的影响不同。在 GMSCs 中，趋化因子 CXCL2 被发现由气溶胶下调，而由液体上调。综合分析表明，电子烟液引起的 CXCL2 上调涉及 H3K27me3 减少和远端增强子激活。另一方面，气溶胶暴露维持 H3K27me3 水平，而直接电子烟液暴露导致全基因组 H3K27me3 减少，特别是在增强子区域。总体而言，电子烟的特定输送方法和成分导致口腔干细胞的转录组和表观基因组发生独特变化。
电子烟对口腔干细胞的影响与烟草烟雾不同。它们的气溶胶和液体对口腔细胞中的基因表达和调控景观有不同的影响。多组学方法对于了解电子烟成分引起的分子变化很重要。这有助于进行毒理学评估并确定它们对牙周健康的影响。转录组和表观基因组谱分析是研究细胞对电子烟反应中涉及的独特分子机制的有力工具。
