MicroRNA expression profiling of nicotine-treated human periodontal ligament cells

Abstract

Cigarette smoking is a lifestyle-related risk factor involved in the causation and progression of periodontal disease. Nicotine is a key toxic component of tobacco. However, the mechanisms underlying nicotine-induced periodontitis have not yet been fully elucidated. The present study investigated the microRNA (miRNA) expression profile of human periodontal ligament cells (PDLCs) treated with nicotine. Using differential analysis of miRNA array data, several differentially expressed miRNAs were identified in nicotine-treated PDLCs. Quantitative real-time PCR was employed to verify the accuracy of the miRNA array, and the targets of these dysregulated miRNAs were further analyzed. Function and pathway enrichment of differentially expressed miRNAs suggested that several important signaling pathways, such as the Toll-like receptor signaling pathway, nicotine addiction, the transforming growth factor-beta signaling pathway, and the hypoxia inducible factor-1 signaling pathway, are potentially responsible for nicotine-induced periodontitis. This study has helped to clarify the epigenetic mechanisms of nicotine-induced periodontitis, highlighting novel biomarkers and therapeutic targets.

MiR-6511b-5p suppresses metastasis of pMMR colorectal cancer through methylation of CD44 by directly targeting BRG1

“…In rheumatoid arthritis, miR-6511b-5p in serum exosomes was positively correlated with clinical remission [ 35 ]. In addition, miR-6511b-5p was detected up-regulated in nicotine-treated human periodontal ligament cells, but the underlying mechanisms were still unknown [ 36 ]. In this study, we explored the potential role of miR-6511b-5p in pMMR colorectal cancer.…”

Emerging Oral Nicotine Products and Periodontal Diseases

“…Smoking, as a risk factor for periodontal disease, may infuence the disease causation and progression through dysregulating miRNAs expression. In vitro study shows nicotine-treated human periodontal ligament cells (PDLCs) presented miRNAs upregulations and downregulations [52]. Tose miRNAs involve in the dysfunction of biological processes, molecular function, cellular components, and signaling pathway e.g., NF-κB, epithelial-mesenchymal signaling, and SMAD signaling [52,53], suggesting ONPs, nicotine-containing products, has the risk of initiating or deteriorating periodontal disease through miRNAs mechanism leading to oral submucous fbrosis.…”

Epigenetics in susceptibility, progression, and diagnosis of periodontitis

“…SOCS1 promoter methylation was observed in 33.3% of smoker samples and only appeared in 4.76% of non-smoker samples. Comprehensive analysis of changes in miRNA expression by nicotine treatment in PDL cells showed that the miRNA regulated Toll-like receptor signaling pathway, nicotine addiction, the transforming growth factor-β signaling pathway, and the hypoxia inducible factor-1 pathway were selectively detected compared with non-treated PDL cells [76] . These results suggest that smoking affects the local epigenetic status in periodontal tissue; however, only one pilot study (sample number = 5 per group) [71] and one epigenome-wide association study (sample number = 18 current smoker) [72] have been reported so far.…”