POSSIBLE ROLE OF PLASMINOGEN ACTIVATOR INHIBITOR-1 IN BRONCHIAL ASTHMA

Abstract

Asthma represents a chronic inflammatory process of airways. Chronic asthma may lead to irreversible airway structural changes characterized by subepithelial fibrosis, extracellular matrix (ECM) deposition, smooth muscle hypertrophy, and goblet cell hyperplasia in the airways, defined as airway remodeling. However, there is a surprising lack of fibrosis or connective tissue

destruction in asthma compared to other chronic inflammatory or obstructive diseases of the airway that involve neutrophils, suggesting the existence of protective mechanisms against fibrosis and reversal of fibrosis in the eosinophilic inflammation of asthma. Plasmingen activator inhibitor (PAI)-1 is the main inhibitor of the

fuibrinolytic system, and is known to play an essential role in tissue remodeling. The fibrinolytic system comprises an inactive pro-enzyme plasminogen, which is converted to the active enzyme, plasmin, which degrades fibrin into soluble fibrin degradation products. Two immunologically distinct physiologic plasminogen activators have been identified in blood, tissue plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA). The tissue- type plasminogen activator (tPA) and urokinase- type plasminogen activator (uPA) convert plasminogen to plasmin, which enhances proteolytic degradation of the extracellular matrix (ECM).