ArticleBMC pulmonary medicine2014
mAChRs activation induces epithelial-mesenchymal transition on lung epithelial cells.
Article in BMC pulmonary medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- The Roles of Acetylcholine and Muscarinic Receptors in Allergic Rhinitis: Mechanisms, Clinical Insights and Future Directions.Current allergy and asthma reports · 2025Review
- OCTN1 mediates acetylcholine transport in the A549 lung cancer cells: possible pathophysiological implications.Frontiers in molecular biosciences · 2024Article
- Atropine Is a Suppressor of Epithelial-Mesenchymal Transition (EMT) That Reduces Stemness in Drug-Resistant Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Muscarinic Receptors Associated with Cancer.Cancers · 2022Review
- Biological behaviors of muscarinic receptors in mesenchymal stem cells derived from human placenta and bone marrow.Iranian journal of basic medical sciences · 2020Article
- Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway.Toxins · 2019Article
- Acetylcholine signaling system in progression of lung cancers.Pharmacology & therapeutics · 2019Review
- Role of Muscarinic Acetylcholine Receptors in Breast Cancer: Design of Metronomic Chemotherapy.Current clinical pharmacology · 2019Review
- Airway epithelial barrier dysfunction in the pathogenesis and prognosis of respiratory tract diseases in childhood and adulthood.Tissue barriers · 2017Review
- The effects of substance P and acetylcholine on human tenocyte proliferation converge mechanistically via TGF-β1.PloS one · 2017Article
- The activation of M3 mAChR in airway epithelial cells promotes IL-8 and TGF-β1 secretion and airway smooth muscle cell migration.Respiratory research · 2016Article
- Role of acetylcholinesterase in lung cancer.Thoracic cancer · 2015Review
- Effects of Electroacupuncture on Chronic Unpredictable Mild Stress Rats Depression-Like Behavior and Expression of p-ERK/ERK and p-P38/P38.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Epithelial mesenchymal transition in smokers: large versus small airways and relation to airflow obstruction.International journal of chronic obstructive pulmonary disease · 2015Article
- Clinical significance of epithelial mesenchymal transition (EMT) in chronic obstructive pulmonary disease (COPD): potential target for prevention of airway fibrosis and lung cancer.Clinical and translational medicine · 2014Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial-mesenchymal transition (EMT) has been proposed as a mechanism in the progression of airway diseases and cancer. Here, we explored the role of acetylcholine (ACh) and the pathway involved in the process of EMT, as well as the effects of mAChRs antagonist.
methodsHuman lung epithelial cells were stimulated with carbachol, an analogue of ACh, and epithelial and mesenchymal marker proteins were evaluated using western blot and immunofluorescence analyses.
resultsDecreased E-cadherin expression and increased vimentin and α-SMA expression induced by TGF-β1 in alveolar epithelial cell (A549) were significantly abrogated by the non-selective mAChR antagonist atropine and enhanced by the acetylcholinesterase inhibitor physostigmine. An EMT event also occurred in response to physostigmine alone. Furthermore, ChAT express and ACh release by A549 cells were enhanced by TGF-β1. Interestingly, ACh analogue carbachol also induced EMT in A549 cells as well as in bronchial epithelial cells (16HBE) in a time- and concentration-dependent manner, the induction of carbachol was abrogated by selective antagonist of M1 (pirenzepine) and M3 (4-DAMP) mAChRs, but not by M2 (methoctramine) antagonist. Moreover, carbachol induced TGF-β1 production from A549 cells concomitantly with the EMT process. Carbachol-induced EMT occurred through phosphorylation of Smad2/3 and ERK, which was inhibited by pirenzepine and 4-DAMP.
conclusionsOur findings for the first time indicated that mAChR activation, perhaps via M1 and M3 mAChR, induced lung epithelial cells to undergo EMT and provided insights into novel therapeutic strategies for airway diseases in which lung remodeling occurs.
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