ArticleThe Journal of allergy and clinical immunology2016
The cardiomyocyte protein αT-catenin contributes to asthma through regulating pulmonary vein inflammation.
Article in The Journal of allergy and clinical immunology, 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, 15 citations in OpenAlex.
- Intravital imaging of pulmonary lymphatics in inflammation and metastatic cancer.The Journal of experimental medicine · 2025Article
- Widespread mutagenesis and chromosomal instability shape somatic genomes in systemic sclerosis.Nature communications · 2024Article
- Intravital imaging of pulmonary lymphatics in inflammation and metastatic cancer.bioRxiv : the preprint server for biology · 2024Article
- Alpha-T-catenin is expressed in peripheral nerves as a constituent of Schwann cell adherens junctions.Biology open · 2022Article
- Free Feeding of CpG-Oligodeoxynucleotide Particles Prophylactically Attenuates Allergic Airway Inflammation and Hyperresponsiveness in Mice.Frontiers in immunology · 2021Article
- Exome sequencing in multiple sclerosis families identifies 12 candidate genes and nominates biological pathways for the genesis of disease.PLoS genetics · 2019Article
- αT-catenin: A developmentally dispensable, disease-linked member of the α-catenin family.Tissue barriers · 2018Review
- Cardiomyocytes of the Heart and Pulmonary Veins: Novel Contributors to Asthma?American journal of respiratory cell and molecular biology · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecent genome-wide association studies have identified single nucleotide polymorphisms in the gene encoding the protein αT-catenin (CTNNA3) that correlate with both steroid-resistant atopic asthma and asthmatic exacerbations. α-Catenins are important mediators of cell-cell adhesion, and αT-catenin is predominantly expressed in cardiomyocytes. In the lung αT-catenin appears to be exclusively expressed in cardiomyocytes surrounding the pulmonary veins (PVs), but its contribution to atopic asthma remains unknown.
objectiveWe sought to understand the role of αT-catenin in asthma pathogenesis.
methodsWe used αT-catenin knockout mice and a house dust mite (HDM) extract model of atopic asthma, with assessment by means of forced oscillation, bronchoalveolar lavage, and histologic analysis.
resultsWe found that the genetic loss of αT-catenin in mice largely attenuated HDM-induced airway inflammation and airway hyperresponsiveness to methacholine. Mice lacking αT-catenin that were exposed to HDM extract had reduced PV inflammation, specifically near the large veins surrounded by cardiac cells. The proximity of the airways to PVs correlated with the severity of airway goblet cell metaplasia, suggesting that PVs can influence the inflammatory milieu of adjacent airways. Loss of αT-catenin led to compensatory upregulation of αE-catenin, which itself has a defined anti-inflammatory function.
conclusionThese data mechanistically support previous clinical and genetic associations between αT-catenin and the development of atopic asthma and suggest that PVs might have an underappreciated role in allergic airway inflammation.
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