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Published ahead of print on September 22, 2005, doi:10.1164/rccm.200406-703OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 1, January 2006, 32-41

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Submitted on June 3, 2004
Accepted on September 20, 2005

Connective Tissue Growth Factor Induces Extracellular Matrix in Asthmatic Airway Smooth Muscle

Peter R.A. Johnson1, Janette K Burgess1*, Qi Ge2, Maree Poniris2, Sarah Boustany3, Stephen M Twigg4, and Judith L Black1

1 Department of Pharmacology, University of Sydney, Sydney, NSW, Australia; Woolcock Institute for Medical Research, Royal Prince Alfred Hospital, Sydney, NSW, Australia, 2 Department of Pharmacology, University of Sydney, Sydney, NSW, Australia, 3 Woolcock Institute for Medical Research, Royal Prince Alfred Hospital, Sydney, NSW, Australia, 4 Discipline of Medicine, University of Sydney, Sydney, NSW, Australia; Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, NSW, Australia

* To whom correspondence should be addressed. E-mail: Janette{at}pharmacol.usyd.edu.au.

Transforming growth factor {beta} and connective tissue growth factor may be implicated in extracellular matrix protein deposition in asthma. We have recently reported that transforming growth factor {beta} increased connective tissue growth factor expression in airway smooth muscle cells isolated from asthmatic patients. In this study we examined fibronectin and collagen production and signal transduction pathways following stimulation with transforming growth factor {beta} and connective tissue growth factor. In both asthmatic and nonasthmatic airway smooth muscle cells, transforming growth factor {beta} and connective tissue growth factor led to the production of fibronectin and collagen I. Fibronectin and collagen expression was extracellular regulated kinase dependent in both cell types but phosphoinositide-3 kinase dependent only in asthmatic airway smooth muscle cells. p38 was implicated in fibronectin but not collagen expression in both cell types. Transforming growth factor {beta} induction of fibronectin and collagen was in part mediated by an autocrine action of connective tissue growth factor. Phosphorylation of SMAD-2 may represent an additional pathway as this was increased in asthmatic cells. Our results suggest that these two cytokines may be important in the deposition of extracellular matrix proteins and that the signal transduction pathways may be different in asthmatic and non-asthmatic cells.
Key words: Asthma, extracellular matrix, transforming growth factor beta, connective tissue growth factor




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