ArticleJournal of thoracic disease2018
Neurokinin 1 receptor promotes rat airway smooth muscle cell migration in asthmatic airway remodelling by enhancing tubulin expression.
Article in Journal of thoracic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Small airway disease as a key factor in COPD: new perspectives and insights.Frontiers in medicine · 2025Review
- Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Stigmasterol alleviates allergic airway inflammation and airway hyperresponsiveness in asthma mice through inhibiting substance-P receptor.Pharmaceutical biology · 2023Article
- NORAD Promotes the Viability, Migration, and Phenotypic Switch of Human Vascular Smooth Muscle Cells during Aortic Dissection via LIN28B-Mediated TGF-BioMed research international · 2022Article
- Network and co-expression analysis of airway smooth muscle cell transcriptome delineates potential gene signatures in asthma.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway remodelling is a major contributor to hyper-responsiveness leading to chronic asthma; however, the underlying mechanisms remain unclear. This study aimed to investigate the effects of a neurokinin 1 receptor (NK1R) antagonist (WIN62577) on the migration of airway smooth muscle cells (ASMCs) and the expression of NK1R and alpha-tubulin in airway remodelling using young rats with asthma.
methodsSprague-Dawley rats were randomly divided into a control group and airway remodelling group. Rats in the model group were stimulated with ovalbumin for 8 weeks. Primary ASMCs were cultured and purified from all rats, and then treated with different doses of WIN62577. The expression of NK1R and α-tubulin in ASMCs was assessed using immunofluorescence, real-time quantitative polymerase chain reaction, and western blotting. Changes in ASMC migration were detected by a transwell chamber assay.
resultsThe transwell assay showed that the number of migrating ASMCs in the asthmatic airway remodelling group was significantly greater than that in the control group (P<0.01), which was inhibited by WIN62577 in a dose-dependent manner, with peak inhibition detected at 10
conclusionsNK1R antagonists may suppress ASMC migration in a rat model of airway remodelling by inhibiting tubulin expression, indicating a new potential target for the treatment and control of chronic asthma.
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Registered trials
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