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Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition

Eapen, Mathew Suji, Lu, Wenying, Hackett, Tillie L, Singhera, Gupreet Kaur, Mahmood, Malik Quasir, Hardikar, Ashutosh, Ward, Chris, Walters, Eugene H and Sohal, Sukhwinder Singh 2021, 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, vol. 7, no. 2, pp. 1-12, doi: 10.1183/23120541.00876-2020.

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Title Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition
Author(s) Eapen, Mathew Suji
Lu, Wenying
Hackett, Tillie L
Singhera, Gupreet Kaur
Mahmood, Malik Quasir
Hardikar, Ashutosh
Ward, Chris
Walters, Eugene H
Sohal, Sukhwinder Singh
Journal name ERJ open research
Volume number 7
Issue number 2
Article ID 00876-2020
Start page 1
End page 12
Total pages 12
Publisher European Respiratory Society (ERS)
Place of publication Sheffield, Eng.
Publication date 2021-04
ISSN 2312-0541
2312-0541
Summary Introduction Previous reports have shown epithelial–mesenchymal transition (EMT) as an active process that contributes to small airway fibrotic pathology. Myofibroblasts are highly active pro-fibrotic cells that secrete excessive and altered extracellular matrix (ECM). Here we relate small airway myofibroblast presence with airway remodelling, physiology and EMT activity in smokers and COPD patients. Methods Lung resections from nonsmoker controls, normal lung function smokers and COPD current and ex-smokers were stained with anti-human α-smooth muscle actin (SMA), collagen 1 and fibronectin. αSMA+ cells were computed in reticular basement membrane (Rbm), lamina propria and adventitia and presented per mm of Rbm and mm2 of lamina propria. Collagen-1 and fibronectin are presented as a percentage change from normal. All analyses including airway thickness were measured using Image-pro-plus 7.0. Results We found an increase in subepithelial lamina propria (especially) and adventitia thickness in all pathological groups compared to nonsmoker controls. Increases in αSMA+ myofibroblasts were observed in subepithelial Rbm, lamina propria and adventitia in both the smoker and COPD groups compared to nonsmoker controls. Furthermore, the increase in the myofibroblast population in the lamina propria was strongly associated with decrease in lung function, lamina propria thickening, increase in ECM protein deposition, and finally EMT activity in epithelial cells. Conclusions This is the first systematic characterisation of small airway myofibroblasts in COPD based on their localisation, with statistically significant correlations between them and other pan-airway structural, lung function and ECM protein changes. Finally, we suggest that EMT may be involved in such changes.
Language eng
DOI 10.1183/23120541.00876-2020
Indigenous content off
HERDC Research category C1 Refereed article in a scholarly journal
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30152910

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Open Access Collection
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.