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Articles in PresS, published online ahead of print December 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00091.2002
Submitted on March 26, 2002
Accepted on November 26, 2002
receptors
1 Department of Medicine, University of British Columbia, Vancouver, BC, Canada
2 Department of Cell Biology & Anatomy, University of Miami, Miami, FL, USA
3 GlaxoSmithKline, Stevenage, Herts, United Kingdom
* To whom correspondence should be addressed. E-mail: nasreen.khalil{at}bccdc.ca.
Fibrosis around the smooth muscle of asthmatic airway walls leads to irreversible airway obstruction. Bronchial epithelial cells release GM-CSF in asthmatics and are in
close proximity to airway smooth muscle cells (ASMC). The findings in this study demonstrate that GM-CSF induces confluent prolonged serum deprived cultures of ASMC to increase expression of collagen I and fibronectin. GM-CSF also induced ASMC to increase the expression of TGF-
receptors type I, II and III (TR-I, TR-II, TR-III), but had no detectable effect on the release of TGF-1 by the same ASMC. The
presence of GM-CSF also induced the association of TGF-1 with TR-III, which enhances binding of TGF-1 to TR-II. The induction of TRs was parallel to the increased induction of phosphorylated Smad-2 (p-Smad-2) and CTGF, indicative of
TGF- mediated connective tissue synthesis. Dexamethasone decreased GM-CSF induced TR-I, TR-II, TR-III, p-Smad-2, CTGF, collagen I and fibronectin. In conclusion, GM-CSF increases the responsiveness of ASMC to TGF- 1 mediated
connective tissue expression by induction of TRs, which is inhibited by corticosteroids.
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