ArticleScientific reports2019
Tensin1 expression and function in chronic obstructive pulmonary disease.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Interactive Effects of Genetic Susceptibility and Early-Life Tobacco Smoke Exposure on the Asthma-Eczema Complex Phenotype in Children: 6-Year Follow-Up Case-Control Study.International journal of molecular sciences · 2025Article
- Hederasaponin C ameliorates chronic obstructive pulmonary disease pathogenesis by targeting TLR4 to inhibit NF-κB/MAPK signaling pathways.Chinese medicine · 2025Article
- Identification of Novel Biomarkers Associated with Corticosteroid Resistance in Asthma by Bioinformatics Analysis and Experimental Validation.Journal of inflammation research · 2025Article
- KDELR2 is necessary for chronic obstructive pulmonary disease airway Mucin5AC hypersecretion via an IRE1α/XBP-1s-dependent mechanism.Journal of cellular and molecular medicine · 2024Article
- TNS1 and NRXN1 Genes Interacting With Early-Life Smoking Exposure in Asthma-Plus-Eczema Susceptibility.Allergy, asthma & immunology research · 2023Article
- The progress of research into pseudophosphatases.Frontiers in public health · 2022Review
- The Roles of Pseudophosphatases in Disease.International journal of molecular sciences · 2021Review
- Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial-mesenchymal transition.ERJ open research · 2021Article
- The Potential Role and Regulatory Mechanisms of MUC5AC in Chronic Obstructive Pulmonary Disease.Molecules (Basel, Switzerland) · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) constitutes a major cause of morbidity and mortality. Genome wide association studies have shown significant associations between airflow obstruction or COPD with a non-synonymous SNP in the TNS1 gene, which encodes tensin1. However, the expression, cellular distribution and function of tensin1 in human airway tissue and cells are unknown. We therefore examined these characteristics in tissue and cells from controls and people with COPD or asthma. Airway tissue was immunostained for tensin1. Tensin1 expression in cultured human airway smooth muscle cells (HASMCs) was evaluated using qRT-PCR, western blotting and immunofluorescent staining. siRNAs were used to downregulate tensin1 expression. Tensin1 expression was increased in the airway smooth muscle and lamina propria in COPD tissue, but not asthma, when compared to controls. Tensin1 was expressed in HASMCs and upregulated by TGFβ1. TGFβ1 and fibronectin increased the localisation of tensin1 to fibrillar adhesions. Tensin1 and α-smooth muscle actin (αSMA) were strongly co-localised, and tensin1 depletion in HASMCs attenuated both αSMA expression and contraction of collagen gels. In summary, tensin1 expression is increased in COPD airways, and may promote airway obstruction by enhancing the expression of contractile proteins and their localisation to stress fibres in HASMCs.
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