ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Nicotinic acetylcholine receptor expression in human airway correlates with lung function.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A systematic review of possible serious adverse health effects of nicotine replacement therapy.Archives of toxicology · 2017Pooled it
- Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine.Toxicology reports · 2026Article
- The CHRNA5 rs16969968 variant is associated with MMP-9 expression and inflammatory signaling in COPD in a West Bengal population, India.Frontiers in pharmacology · 2026Article
- Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Targeted lung denervation modulates the mucosal epithelial transcriptome in COPD.ERJ open research · 2022Article
- Enhancement of airway ciliary beating mediated via voltage-gated CaPflugers Archiv : European journal of physiology · 2022Article
- Article
- Antioxidant Systems, lncRNAs, and Tunneling Nanotubes in Cell Death Rescue from Cigarette Smoke Exposure.Cells · 2022Review
- Article
- Nicotinic Acetylcholine Receptors in the Respiratory Tract.Molecules (Basel, Switzerland) · 2021Review
- Iron-Regulated Reactive Oxygen Species Production and Programmed Cell Death in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2021Article
- Paradoxical effects of cigarette smoke and COPD on SARS-CoV-2 infection and disease.BMC pulmonary medicine · 2021Article
- E-cigarette vape and lung ACE2 expression: Implications for coronavirus vulnerability.Environmental toxicology and pharmacology · 2021Article
- Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle.Archives of biochemistry and biophysics · 2021Article
- Chr15q25 Genetic Variant rs16969968 Alters Cell Differentiation in Respiratory Epithelia.International journal of molecular sciences · 2021Article
- Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity.Molecules (Basel, Switzerland) · 2020Article
- Addressing the challenges of E-cigarette safety profiling by assessment of pulmonary toxicological response in bronchial and alveolar mucosa models.Scientific reports · 2020Article
- Nicotinic Receptor Subunits Atlas in the Adult Human Lung.International journal of molecular sciences · 2020Article
- Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health.International journal of molecular sciences · 2020Review
- GTS-21, an α7nAChR agonist, suppressed the production of key inflammatory mediators by PBMCs that are elevated in COPD patients and associated with impaired lung function.Immunobiology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Nicotine and its derivatives, by binding to nicotinic acetylcholine receptors (nAChRs) on bronchial epithelial cells, can regulate cellular signaling and inflammatory processes. Delineation of nAChR subtypes and their responses to nicotine stimulation in bronchial epithelium may provide information for therapeutic targeting in smoking-related inflammation in the airway. Expression of nAChR subunit genes in 60 bronchial epithelial biopsies and immunohistochemical staining for the subcellular locations of nAChR subunit expression were evaluated. Seven human bronchial epithelial cell lines (HBECs) were exposed to nicotine in vitro for their response in nAChR subunit gene expression to nicotine exposure and removal. The relative normalized amount of expression of nAChR α4, α5, and α7 and immunohistochemical staining intensity of nAChR α4, α5, and β3 expression showed significant correlation with lung function parameters. Nicotine stimulation in HBECs resulted in transient increase in the levels of nAChR α5 and α6 but more sustained increase in nAChR α7 expression. nAChR expression in bronchial epithelium was found to correlate with lung function. Nicotine exposure in HBECs resulted in both short and longer term responses in nAChR subunit gene expression. These results gave insight into the potential of targeting nAChRs for therapy in smoking-related inflammation in the airway.
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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.