scholarly journals Auxin Levels Regulate the Expression of a Wound-Inducible Proteinase Inhibitor II-Chloramphenicol Acetyl Transferase Gene Fusion in Vitro and in Vivo

1989 ◽  
Vol 91 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Andrea Kernan ◽  
Robert W. Thornburg
1994 ◽  
Vol 266 (6) ◽  
pp. L593-L611 ◽  
Author(s):  
M. D. Evans ◽  
W. A. Pryor

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.


1989 ◽  
Vol 17 (12) ◽  
pp. 4877-4877 ◽  
Author(s):  
Brendan W. Wren ◽  
Peter Mullany ◽  
Christopher Clayton ◽  
Soad Tabaqchali

2012 ◽  
Vol 92 (15) ◽  
pp. 3072-3078 ◽  
Author(s):  
Milica M Popovic ◽  
Aleksandra Bulajic ◽  
Danijela Ristic ◽  
Branka Krstic ◽  
Ratko M Jankov ◽  
...  

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