AbstractA different form of lung disease including acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome, bronchiolitis, interstitial lung diseases and drug-induced lung diseases are often associated with alveolar epithelial cell apoptosis. Epithelial cells that are the prime important cell in the alveolar architecture produce fibrinolytic components, such as urokinase-type plasminogen activator (uPA), its receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1), and tumor suppressor protein p53. The increased expression of p53, which is responsible for apoptosis of alveolar epithelial cells, and the other components of the fibrinolytic system, and a decreased alveolar fibrinolysis, are strongly involved in the pathogenesis of ALI. The fibrinolytic system, such as uPA, uPAR and PAI-1 interaction with p53, brings about the regulation of the signaling response, as well as the fibrinolytic properties, which will be useful in maintaining the unity of the cell, and also providing the signals to the cells on whether they undergo apoptosis or survival after ALI.
BAY11‑7082 inhibits the expression of tissue factor and plasminogen activator inhibitor‑1 in type‑II alveolar epithelial cells following TNF‑α stimulation via the NF‑κB pathway
