Abstract
A 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.
Abbreviations
- ALI
acute lung injury
- ATII
alveolar type II
- Bcl-XL
B-cell lymphoma-extra large
- BLM
bleomycin
- CS
cigarette smoke
- CSP
caveolin scaffolding domain
- PAI-1
plasminogen activator inhibitor-1
- uPA
urokinase-type plasminogen activator
- uPAR
urokinase plasminogen activator receptor
- UTR
untranslated region
Acknowledgements
I sincerely acknowledge Dr. Sreerama Shetty, Professor, Cellular and Molecular Biology, UT Health Northeast for mentoring me in the field of acute lung injury and pulmonary fibrosis. Help from my colleague staff members from UT Health Northeast and Yenepoya Research Centre is highly appreciated.
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© 2016 Institute of Molecular Biology, Slovak Academy of Sciences
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