Abstract
Fibrin deposition occurs in acute and chronic pulmonary injury: in the alveoli-with hyaline membrane disease (HMD); and in the interstitium-with chronic inflammatory conditions such as idiopathic pulmonary fibrosis (IPF). The mechanism underlying fibrin deposition in the lung is unknown, but may involve a disequilibrium of the protease-anti-protease balance in the fibrinolytic pathway. We have isolated and partially characterized a 50 kDA protein from multiple components of developing lungs-fetal bronchoalveolar lavage (BAL), fetal primary type II cells in culture and fetal lung fibroblasts (WI38, IMR90) in culture-which is a plasminogen activator inhibitor (PAD as demonstrated by reverse fibrin autography (RFA). We have also isolated a 57 kDA protein from these same sources that is a plasminogen activator (PA). We investigated the PA/PAI balance during hyperoxia both in vivo-in BAL from newborn rabbit pups exposed to F1O2 85%; and in vitro-in serum-free conditioned media collected from fetal lung fibroblasts (WI-38) exposed to oxygen concentrations from 21 to 95%. BAL after hyperoxia demonstrates a predominance of PA with little PAI detectable. In contrast, fetal lung fibroblasts exposed to oxygen concentrations for 24, 18 or 72 hours produced primarily a PAI. We conclude that hyperoxia alters the balance of PA and PAI in the lung. We speculate that the predominance of PAI may favor fibrin deposition in the interstitital component.
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Parton, L., Warburton, D., Bowman, C. et al. HYPEROXIA CAUSES DISEQUILIBRIUM IN THE REGULATORS OF FIBRINOLYSIS IN THE LUNG. Pediatr Res 21 (Suppl 4), 219 (1987). https://doi.org/10.1203/00006450-198704010-00319
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DOI: https://doi.org/10.1203/00006450-198704010-00319