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Am J Physiol Lung Cell Mol Physiol 279: L707-L715, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 4, L707-L715, October 2000

Regulation of plasminogen activator inhibitor-1 and urokinase by hyaluronan fragments in mouse macrophages

Maureen R. Horton1, Mitchell A. Olman2, Clare Bao1, Kimberly E. White2, Augustine M. K. Choi3,4, Beek-Yok Chin3,4, Paul W. Noble3,4, and Charles J. Lowenstein1

1 Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; 2 Department of Medicine, University of Alabama School of Medicine, Birmingham, Alabama 35294; 3 Department of Internal Medicine, Yale University School of Medicine, New Haven 06520; and 4 Department of Internal Medicine, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut 06516

Pulmonary inflammation and fibrosis are characterized by increased turnover and production of the extracellular matrix as well as an impairment of lung fibrinolytic activity. Although fragments of the extracellular matrix component hyaluronan induce macrophage production of inflammatory mediators, the effect of hyaluronan on the fibrinolytic mediators plasminogen activator inhibitor (PAI)-1 and urokinase-type plasminogen activator (uPA) is unknown. This study demonstrates that hyaluronan fragments augment steady-state mRNA, protein, and inhibitory activity of PAI-1 as well as diminish the baseline levels of uPA mRNA and inhibit uPA activity in an alveolar macrophage cell line. Hyaluronan fragments alter macrophage expression of PAI-1 and uPA at the level of gene transcription. Similarly, hyaluronan fragments augment PAI-1 and diminish uPA mRNA levels in freshly isolated inflammatory alveolar macrophages from bleomycin-treated rats. These data suggest that hyaluronan fragments influence alveolar macrophage expression of PAI-1 and uPA and may be a mechanism for regulating fibrinolytic activity during lung inflammation.

extracellular matrix; lung; chronic fibrosis


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