ArticleCell proliferation2007
Nicotine-induced proliferation of isolated rat pancreatic acinar cells: effect on cell signalling and function.
Article in Cell proliferation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Effects of a natural polyphenol on nicotine-induced pancreatic cancer cell proliferation.Tobacco induced diseases · 2018Article
- Impact of cigarette smoking on recurrence of hyperlipidemic acute pancreatitis.World journal of gastroenterology · 2017Article
- Epidemiologic and Mechanistic Associations Between Smoking and Pancreatitis.Current treatment options in gastroenterology · 2015Article
- Review
- Axonal guidance signaling pathway interacting with smoking in modifying the risk of pancreatic cancer: a gene- and pathway-based interaction analysis of GWAS data.Carcinogenesis · 2014Article
- Clinical significance of serum COL6A3 in pancreatic ductal adenocarcinoma.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2014Article
- Smoking and Pancreatic Disease.Journal of cancer therapy · 2013Article
- Effect of nicotine on exocytotic pancreatic secretory response: role of calcium signaling.Tobacco induced diseases · 2013Article
- Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- The pathobiological impact of cigarette smoke on pancreatic cancer development (review).International journal of oncology · 2012Review
- Nicotine promotes proliferation of human nasopharyngeal carcinoma cells by regulating α7AChR, ERK, HIF-1α and VEGF/PEDF signaling.PloS one · 2012Article
- The emerging role of smoking in the development of pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2011Review
- Epigenetic effects and molecular mechanisms of tumorigenesis induced by cigarette smoke: an overview.Journal of oncology · 2011Article
- Article
- Induction of osteopontin expression by nicotine and cigarette smoke in the pancreas and pancreatic ductal adenocarcinoma cells.International journal of cancer · 2009Article
- Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection.Pharmacological reviews · 2009Review
- Mitogenic and functional responses by nicotine and hydrogen peroxide in AR42J cells: a comparative study.Tobacco induced diseases · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe aim of the current study was to investigate whether nicotine treatment would induce the proliferation of isolated rat primary pancreatic acinar cells in culture by activating mitogen-activated protein kinase (MAPK) signalling and exocrine secretion. MATERIALS AND
methodsA nicotine dose- and time-response curve was initially developed to determine the optimal dose and time used for all subsequent studies. Proliferation studies were conducted by cell counting and confirmed further by bromodeoxyuridine (BrdU) incorporation and flow cytometry assays. MAPK signalling studies were conducted by Western blot analysis. Localization of ERK1/2 signals, with or without nicotine and the MAPK inhibitor, was visualized by immunofluorescence.
resultsNicotine treatment caused dose-dependent activation of extracellular signal-regulated kinases (ERK1/2), the maxima occurring at 100 micro m and at 3 min after treatment; the response was suppressed by the ERK1/2 inhibitor. Maximal nicotine-induced cell proliferation occurred at 24 h, and UO126-treatment significantly reduced this response. Exposure of cells to 100 microm nicotine for 6 min significantly enhanced both baseline and cholecystokinin-stimulated cell function, and these effects were not affected by treatment with the inhibitor of ERK1/2 but were suppressed by mecamylamine, a nicotinic receptor antagonist.
conclusionsOur results suggest that nicotine treatment induced cell proliferation of isolated pancreatic acinar cells and that this is coupled with the activation of MAPK signalling with no effect on its function. Hence, in primary cells, the mechanism of induction and regulation of these two processes, cell proliferation and cell function, by nicotine treatment are independent of each other.
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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.