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Am J Physiol Lung Cell Mol Physiol 274: L499-L507, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 4, L499-L507, April 1998

Dexamethasone activates expression of the PDGF-alpha receptor and induces lung fibroblast proliferation

G. Sakuntala Warshamana, Sylvia Martinez, Joseph A. Lasky, Miriam Corti, and Arnold R. Brody

Lung Biology Program and Departments of Pathology and Medicine, Tulane University Medical Center, New Orleans, Louisiana 70112

Corticosteroids (CSs) are commonly used for anti-inflammatory therapy in asthma and in interstitial lung diseases. In attempting to understand the mechanisms through which CSs control cell proliferation, we have carried out experiments to test the effects of dexamethasone (Dex) on the growth of lung fibroblasts. Using mouse 3T3 fibroblasts as well as early-passage rat lung fibroblasts (RLFs), we show that the quiescent cells in 1% serum or in serum-free media proliferate significantly in response to the addition of 10-7 to 10-9 M Dex. Increases as high as fourfold in cell numbers were recorded for the RLFs after 48 h in culture. A polyclonal antibody to the AB isoform of human platelet-derived growth factor (PDGF) blocked the proliferative response. As expected, the fibroblasts produced primarily PDGF-A chain, and the RLFs exhibited few PDGF-alpha receptors (PDGF-Ralpha ), the receptor type necessary for binding the AA isoform. Accordingly, we determined that Dex upregulated PDGF-Ralpha mRNA and protein. Therefore, we can postulate that Dex-induced fibroblast proliferation is mediated, at least in part, by PDGF-AA, which binds to the PDGF-Ralpha .

platelet-derived growth factor-alpha receptor; platelet-derived growth factor isoforms; anti-platelet-derived growth factor


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