ArticleAllergy2013
Endothelin-1 directs airway remodeling and hyper-reactivity in a murine asthma model.
Article in Allergy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanism of RNA-Binding Protein ELAVL1 in Promoting Th2 Cell Differentiation Through Stabilizing CPA3 mRNA in Allergic Rhinitis.The Kaohsiung journal of medical sciences · 2026Article
- The Dual Role of the Airway Epithelium in Asthma: Active Barrier and Regulator of Inflammation.Cells · 2023Review
- Rhinovirus infection induces secretion of endothelin-1 from airway epithelial cells in both in vitro and in vivo models.Respiratory research · 2023Article
- Endothelin-1 induces connective tissue growth factor expression in human lung fibroblasts by disrupting HDAC2/Sin3A/MeCP2 corepressor complex.Journal of biomedical science · 2023Article
- MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling.The Journal of biological chemistry · 2020Article
- Airway mechanical compression: its role in asthma pathogenesis and progression.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Transcriptomic analysis reveals diverse gene expression changes in airway macrophages during experimental allergic airway disease.Wellcome open research · 2020Article
- Inhibition of airway remodeling and inflammatory response by Icariin in asthma.BMC complementary and alternative medicine · 2019Article
- Endothelin-1 mediates Aspergillus fumigatus-induced airway inflammation and remodelling.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Article
- Insulin resistance mediates high-fat diet-induced pulmonary fibrosis and airway hyperresponsiveness through the TGF-β1 pathway.Experimental & molecular medicine · 2019Article
- Regulatory cytokine function in the respiratory tract.Mucosal immunology · 2019Review
- Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Article
- Airway epithelial compression promotes airway smooth muscle proliferation and contraction.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Type 2 immunity in tissue repair and fibrosis.Nature reviews. Immunology · 2018Review
- Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?American journal of respiratory cell and molecular biology · 2017Review
- Pulmonary Epithelial Cell-Derived Cytokine TGF-β1 Is a Critical Cofactor for Enhanced Innate Lymphoid Cell Function.Immunity · 2015Article
- IL-25 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma model.Respiratory research · 2015Article
- Epigenetics of hyper-responsiveness to allergen challenge following intrauterine growth retardation rat.Respiratory research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe current paradigm describing asthma pathogenesis recognizes the central role of abnormal epithelial function in the generation and maintenance of the disease. However, the mechanisms responsible for the initiation of airway remodeling, which contributes to decreased lung function, remain elusive. Therefore, we aimed to determine the role of altered pulmonary gene expression in disease inception and identify proremodeling mediators.
methodsUsing an adenoviral vector, we generated mice overexpressing smad2, a TGF-β and activin A signaling molecule, in the lung. Animals were exposed to intranasal ovalbumin (OVA) without systemic sensitization.
resultsControl mice exposed to inhaled OVA showed no evidence of pulmonary inflammation, indices of remodeling, or airway hyper-reactivity. In contrast, local smad2 overexpression provoked airway hyper-reactivity in OVA-treated mice, concomitant with increased airway smooth muscle mass and peribronchial collagen deposition. Pulmonary eosinophilic inflammation was not evident, and there was no change in serum IgE or IgG1 levels. The profound remodeling changes were not mediated by classical pro-inflammatory Th2 cytokines. However, uric acid and interleukin-1β levels in the lung were increased. Epithelial-derived endothelin-1 and fibroblast growth factor were also augmented in smad2-expressing mice. Blocking endothelin-1 prevented these phenotypic changes.
conclusionsInnate epithelial-derived mediators are sufficient to drive airway hyper-reactivity and remodeling in response to environmental insults in the absence of overt Th2-type inflammation in a model of noneosinophilic, noninflammed types of asthma. Targeting potential asthma therapies to epithelial cell function and modulation of locally released mediators may represent an effective avenue for therapeutic design.
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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.