ArticleJournal of molecular medicine (Berlin, Germany)2017
Nicotine protects against DSS colitis through regulating microRNA-124 and STAT3.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- SerumInternational journal of molecular sciences · 2026Article
- Neuroimmune interactions in inflammatory bowel disease: Role of intestinal macrophages and the cholinergic pathway.World journal of gastroenterology · 2025Review
- Nicotine Attenuates Chondrocyte Inflammation via the α7nAChR-Mediated Inhibition of the HMGB1/TLR4/NF-κB Signaling Pathway.Journal of inflammation research · 2025Article
- The Bidirectional Gut-Lung Axis in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2023Review
- Tobacco Alkaloid Assessment in a DSS-Induced Colitis Mouse Model with a Fully Humanized Immune System.International journal of molecular sciences · 2023Article
- miRNA Molecules-Late Breaking Treatment for Inflammatory Bowel Diseases?International journal of molecular sciences · 2023Review
- The role of microRNAs in nicotine signaling.EXCLI journal · 2023Review
- How autophagy, a potential therapeutic target, regulates intestinal inflammation.Frontiers in immunology · 2023Review
- Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models.International journal of molecular sciences · 2022Review
- Associations Between Smoking and Primary Sjögren Syndrome Classification Using the Sjögren's International Collaborative Clinical Alliance Cohort.ACR open rheumatology · 2022Article
- Environmental Impact on the Epigenetic Mechanisms Underlying Parkinson's Disease Pathogenesis: A Narrative Review.Brain sciences · 2022Review
- The potential for traditional Chinese therapy in treating sleep disorders caused by COVID-19 through the cholinergic anti-inflammatory pathway.Frontiers in pharmacology · 2022Review
- Bioelectronics in the brain-gut axis: focus on inflammatory bowel disease (IBD).International immunology · 2021Review
- Nicotine and its metabolite cotinine target MD2 and inhibit TLR4 signaling.Innovation (Cambridge (Mass.)) · 2021Article
- The Role of microRNAs in Development of Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2021Review
- MicroRNA-181a Is Involved in Methamphetamine Addiction Through the ERAD Pathway.Frontiers in molecular neuroscience · 2021Article
- Intestinal Macrophage Autophagy and its Pharmacological Application in Inflammatory Bowel Disease.Frontiers in pharmacology · 2021Review
- Elevated miR-124-3p in the aging colon disrupts mucus barrier and increases susceptibility to colitis by targeting T-synthase.Aging cell · 2020Article
- Rab27A promotes cellular apoptosis and ROS production by regulating the miRNA-124-3p/STAT3/RelA signalling pathway in ulcerative colitis.Journal of cellular and molecular medicine · 2020Article
- Divergent Effect of Cigarette Smoke on Innate Immunity in Inflammatory Bowel Disease: A Nicotine-Infection Interaction.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although it is generally believed that nicotine accounts for the beneficial effect of smoking on ulcerative colitis, the underlying mechanisms remain not well understood. Our previous finding that nicotine inhibits inflammatory responses through inducing miR-124 prompted us to ask whether the miRNA is involved in the protective action of nicotine against UC. Our present study found that miR-124 expression is upregulated in colon tissues from UC patients and DSS colitis mice. Nicotine treatment further augmented miR-124 expression in lymphocytes isolated from human ulcerative colonic mucosa and ulcerative colon tissues from DSS mice, both in infiltrated lymphocytes and epithelial cells. Moreover, knockdown of miR-124 significantly diminished the beneficial effect of nicotine on murine colitis and IL-6-treated Caco-2 colon epithelial cells. Further analysis indicated that nicotine inhibited STAT3 activation in vivo and in IL-6 treated Caco-2 cells and Jurkat human T lymphocytes, in which miR-124 knockdown led to increased activation of STAT3. Blocking STAT3 activity alone is beneficial for DSS colitis and also abolished nicotine's protective effect in this model. These data indicate that nicotine exerts its protective action in UC through inducing miR-124 and inhibiting STAT3, and suggest that the miR-124/STAT3 system is a potential target for the therapeutic intervention of UC. KEY MESSAGE: Nicotine upregulates miR-124 expression in ulcerative colon tissues and cells. MiR-124 is required for the protective role of nicotine in DSS colitis mice and epithelial cells. The protective effect of nicotine in murine DSS colitis depends on blocking STAT3 activation. MiR-124 mediates the inhibitory role of nicotine on STAT3/p-STAT3. Targeting miR-124 and STAT3 represents a novel approach for treating ulcerative colitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.