ArticleRespiratory research2016
The activation of M3 mAChR in airway epithelial cells promotes IL-8 and TGF-β1 secretion and airway smooth muscle cell migration.
Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Therapeutic responses toScience translational medicine · 2020Trial
- Aberrant PJA2-CHRM3 signaling creates a therapeutic vulnerability in gastric tumor.British journal of cancer · 2025Article
- The Roles of Acetylcholine and Muscarinic Receptors in Allergic Rhinitis: Mechanisms, Clinical Insights and Future Directions.Current allergy and asthma reports · 2025Review
- Estrogen receptors differentially modifies lamellipodial and focal adhesion dynamics in airway smooth muscle cell migration.Molecular and cellular endocrinology · 2024Article
- Bronchial epithelial and airway smooth muscle cell interactions in health and disease.Heliyon · 2023Review
- Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.Journal of asthma and allergy · 2021Review
- Characterizing well-differentiated culture of primary human nasal epithelial cells for use in wound healing assays.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- IL-17A-associated IKK-α signaling induced TSLP production in epithelial cells of COPD patients.Experimental & molecular medicine · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMuscarinic acetylcholine receptors (mAChRs) have been identified in airway epithelium, and epithelium-derived chemokines can initiate the migration of airway smooth muscle (ASM) cells. However, the mAChRs that are expressed in airway epithelium and the mechanism underlying the regulation of ASM cell migration are not clear. The aim of this study was to test whether the effects of the epithelium-derived chemokines on ASM cell migration could be modulated by mAChRs.
methodHuman epithelial cells (A549 cells) were stimulated with cigarette smoke extract (CSE) or the mAChRs agonist carbachol. IL-8 and TGF-β1 production were measured by ELISA, and human ASM cell migration was measured using the transwell migration assay and scratch assay. The mRNA levels of the mAChRs subtypes and the acetylcholine concentrations were measured using RT-PCR and LC-MS/MS, respectively.
resultsASM cell migration toward CSE-stimulated A549 cells was markedly reduced by Ac-RRWWCR-NH2 (IL-8 inhibitor) and SB431542 (TGF-β1 inhibitor). CSE-induced ASM cell migration was also suppressed by the mAChRs antagonist tiotropium. Interestingly, carbachol-stimulated A549 cells also induced ASM cell migration; this migration event was suppressed by tiotropium, Ac-RRWWCR-NH2 and SB431542. In addition, the effects of CSE on ASM cell migration were significantly and cooperatively enhanced by carbachol compared to CSE alone. Carbachol-induced ASM cell migration was reduced by selective inhibitors of PI3K/Akt (LY294002) and p38 (SB203580), suggesting that it occurred through p38 and Akt phosphorylation, which was inhibited by the M3 mAChR antagonist 4-DAMP.
conclusionsThese findings indicate that M3 mAChR may be important therapeutic target for obstructive airway diseases, as it regulates the effects of the epithelial-derived chemokines on ASM cell migration, which results in lung remodeling.
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