ArticleJournal of cellular and molecular medicine2020
Inflammation has synergistic effect with nicotine in periodontitis by up-regulating the expression of α7 nAChR via phosphorylated GSK-3β.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Nicotine destructs dental stem cell-based periodontal tissue regeneration.Journal of dental sciences · 2024Article
- TNFα, IL-6, miR-103a-3p, miR-423-5p, miR-23a-3p, miR-15a-5p and miR-223-3p in the crevicular fluid of periodontopathic patients correlate with each other and at different stages of the disease.Scientific reports · 2023Article
- Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review.Cells · 2022Review
- How the mechanical microenvironment of stem cell growth affects their differentiation: a review.Stem cell research & therapy · 2022Review
- Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects.Frontiers in immunology · 2022Review
- Nicotine regulates autophagy of human periodontal ligament cells through α7 nAchR that promotes secretion of inflammatory factors IL-1β and IL-8.BMC oral health · 2021Article
- Periodontal Inflammation and Systemic Diseases: An Overview.Frontiers in physiology · 2021Review
- Inflammation has synergistic effect with nicotine in periodontitis by up-regulating the expression of α7 nAChR via phosphorylated GSK-3β.Journal of cellular and molecular medicine · 2020Article
- The relationship between periodontal status and rheumatoid arthritis - systematic review.Reumatologia · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis is the leading cause of adult tooth loss, and those who smoke are at an increased risk of developing periodontitis. α7 nicotinic acetylcholine receptor (α7 nAChR) is proposed to mediate the potential synergistic effect of nicotine and inflammation in smoking-related periodontitis. However, this has not been experimentally demonstrated. We isolated and cultured human periodontal ligament stem cells (PDLSCs) from healthy and inflamed tissues. PDLSCs were treated with either inflammatory factors or nicotine. We measured expression of genes that are associated with osteogenic differentiation and osteoclast formation using RT-qPCR and Western blot analyses. Besides, immunohistochemical staining, micro-CT analysis and tartaric acid phosphatase staining were used to measure α7 nAChR expression and function. Inflammation up-regulated α7 nAChR expression in both periodontal ligament tissues and PDLSCs. The up-regulated α7 nAChR contributed to the synergistic effect of nicotine and inflammation, leading to a decreased capability of osteogenic differentiation and increased capability of osteoclast formation-induction of PDLSCs. Moreover, the inflammation-induced up-regulation of α7 nAChR was partially dependent on the level of phosphorylated GSK-3β. This study provides experimental evidence for the pathological development of smoking-related periodontitis and sheds new light on developing inflammation and α7 nAChR-targeted therapeutics to treat and prevent the disease.
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