Collagen remodelling by airway smooth muscle is resistant to steroids and β2-agonists

Bourke, J. E., Li, X., Foster, S. R., Wee, E., Dagher, H., Ziogas, J., Harris, T., Bonacci, J. V. and Stewart, A. G. (2011) Collagen remodelling by airway smooth muscle is resistant to steroids and β2-agonists. European Respiratory Journal, 37 1: 173-182. doi:10.1183/09031936.00008109


Author Bourke, J. E.
Li, X.
Foster, S. R.
Wee, E.
Dagher, H.
Ziogas, J.
Harris, T.
Bonacci, J. V.
Stewart, A. G.
Title Collagen remodelling by airway smooth muscle is resistant to steroids and β2-agonists
Journal name European Respiratory Journal   Check publisher's open access policy
ISSN 0903-1936
1399-3003
Publication date 2011-01-01
Sub-type Article (original research)
DOI 10.1183/09031936.00008109
Open Access Status
Volume 37
Issue 1
Start page 173
End page 182
Total pages 10
Place of publication Lausanne, Switzerland
Publisher European Respiratory Society
Language eng
Subject 2740 Pulmonary and Respiratory Medicine
Abstract Bi-directional interactions between airway smooth muscle (ASM) and the altered extracellular matrix (ECM) may influence airway wall remodelling and ASM function in asthma. We have investigated the capacity of cultured human ASM to reorganise the structure of threedimensional collagen gels and the effects of endothelin (ET)-1 and agents used to treat asthma. Human ASM cells were cast in type I collagen gels. Reductions in gel area over 72 h were determined in the absence and presence of ET-1 and potential inhibitors, steroids and β2-adrenoceptor agonists. Changes in gel wet weights and hydroxyproline content were measured and ASM gel morphology was examined by scanning electron microscopy. Cell density-dependent reductions in gel area were augmented by ET-1, mediated via ETA receptors. This process was not associated with ASM contraction or proliferation, but was consistent with ASM tractional remodelling and migration leading to collagen condensation rather than collagen degradation within gels. The collagen remodelling by ASM was unaffected by salbutamol and/or budesonide. This study demonstrates an additional potential role for ASM in ECM regulation and dysregulation in airways disease that is resistant to steroids and β2-adrenoceptor agonists. Therapy-resistant collagen condensation within ASM bundles may facilitate ECM-ASM interactions and contribute to increased internal airways resistance. Copyright
Keyword Airway smooth muscle
Asthma
Collagen
Endothelin-1
Glucocorticoid
Steroid resistance
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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