Restoration of miR‐1305 relieves the inhibitory effect of nicotine on periodontal ligament‐derived stem cell proliferation, migration, and osteogenic differentiation
Recently, many studies reported that nicotine, a major constituent in the cigarette smoke, hinders the regenerative potentials of human PDLSCs and delays the healing process of periodontal diseases 7. As residential stem cells are known to promote tissue regeneration, the delayed healing of periodontal diseases in cigarette smokers could be attributed to the afflicted PDLSC by nicotine 10. However, the mechanisms that nicotine hinders the regenerative potentials of human PDLSCs remain unclear.
MicroRNAs (miRNAs) are a class of 21–24 nucleotide non‐coding RNA molecules and exist extensively in eukaryotic cells 11. These molecules as post‐transcriptional regulators bind to complementary sequences in the 3′ untranslated region (3′UTR) of target mRNAs, and usually lead to gene silencing 12. To date, over 1000 human miRNAs have been identified that are differentially expressed at high dynamic range in developmental stages, cell types, tissues, and diseases. miRNAs are involved in most biological processes by affecting gene regulation, such as cell proliferation, apoptosis, differentiation, embryogenesis, and carcinogenesis 12. Ng et al. 7 reported that miRNA profile of nicotine‐treated PDLSCs was altered, and miR‐1305 and miR‐18b were significantly upregulated in nicotine‐treated PDLSCs and smoker PDLSCs, which suggested miRNAs might play an important role in the nicotine effects on PDLSCs. In addition, Ng et al. 7 also performed the target gene prediction and found RUNX2, which was associated with bone development and downregulated in the nicotine‐treated PDLSCs, was the potential target of differentially expressed miRNAs, including miR‐1305. However, whether nicotine hinders the regenerative potentials of PDLSCs by increasing miR‐1305 level and further decreasing RUNX2 level is not clear. In this study, we aimed to investigate whether nicotine inhibits PDLSC proliferation, migration, and osteogenic differentiation by increasing miR‐1305 level and decreasing RUNX2 level.