Basic fibroblast growth factor (bfgf) induces expression of the pdgf receptor-[alpha] on human bronchial smooth muscle cells. Bonner, James C., Annette Badgett, Pamela M. Lindroos, and Patrick G. Coin. Airway Inflammation Section, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 and Veterans Affairs Medical Center, Durham, NC 27705
APStracts 3:0145L, 1996.
Bronchial smooth muscle cell (SMC) hyperplasia is a key feature in the pathology of asthma. Platelet-derived growth factor (PDGF) isoforms are SMC mitogens. We investigated the effect of basic fibroblast growth factor (bFGF or FGF-2), transforming growth factor-[beta]1 (TGF-[beta]1), interleukin-1[beta] (IL-1[beta]) and tumor necrosis factor-[alpha] (TNF-[alpha]) on the PDGF receptor system on human bronchial SMC from three different donors. bFGF induced gene expression of the PDGF [alpha]-receptor (PDGF-R[alpha]) 3-fold without altering the PDGF [beta]-receptor (PDGF-R[beta]). IL-1[beta] and TNF-[alpha] did not affect the PDGF receptor system. TGF-[beta]1 down-regulated PDGF-R[alpha] mRNA 60% without changing PDGF-R[beta] mRNA levels. Receptor assays showed that bFGF increased the [125I]PDGF-AA binding site 2-fold, while TGF-[beta]1 reduced [125I]PDGF-AA binding 60%. TGF-[beta]1, but not latent TGF-[beta]1, counteracted the bFGF-induced increase in [125I]PDGF-AA binding. PDGF-AA-stimulated tyrosine phosphorylation on the PDGF-R[alpha] was enhanced following treatment with bFGF. bFGF pretreatment enhanced the mitogenic response of SMC to PDGF-AA and PDGF-AB. These findings suggest that up-regulation of the PDGF-R[alpha] by bFGF could contribute to SMC hyperplasia during chronic airway inflammation in asthma. 

Received 26 December 1996; accepted in final form 5 August 1996.
APS Manuscript Number L376-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996