Related Experiment Videos
Induction of arginase isoforms in the lung during hyperoxia
L G Que1, S P Kantrow, C P Jenkinson
1Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
The American Journal of Physiology
|August 5, 1998
Summary
This study shows that arginase, an enzyme involved in L-ornithine production, is upregulated in the lungs during hyperoxic lung injury and recovery. This suggests arginase plays a role in lung repair processes.
Area of Science:
- Biochemistry
- Pulmonary Medicine
- Cellular Biology
Background:
- L-arginine metabolism involves nitric oxide (NO) synthase (NOS) and arginase, producing NO or L-ornithine and urea, respectively.
- Arginase isoform AI is crucial in the liver's urea cycle, while the function of the AII isoform in extrahepatic organs like the lung is less understood.
- Preliminary findings indicated upregulation of lung arginase AII during hyperoxia, prompting further investigation.
Purpose of the Study:
- To characterize the expression of arginase isoforms (AI and AII) and inducible NOS in the lung during hyperoxic lung injury.
- To assess the functional role of arginase in hyperoxic lung injury and subsequent recovery.
- To investigate the correlation between arginase expression and ornithine decarboxylase, a marker of tissue repair.
Main Methods:
- Male Sprague-Dawley rats were exposed to 100% oxygen (hyperoxia) for 60 hours.
- Western blot analysis was used to determine protein expression and cellular distribution of arginase isoforms AI and AII.
- Arginase and NOS activities were measured, and immunostaining was performed. Ornithine decarboxylase expression was assessed during a recovery phase.
Main Results:
- Both arginase isoforms (AI and AII) protein levels significantly increased (403% and 88%, respectively) after 60 hours of hyperoxia and remained elevated during recovery.
- Arginase activity increased by 37%, while NOS activity remained unchanged and inducible NOS was not detected.
- Increased arginase expression was localized to peribronchial and perivascular connective tissues, and correlated with ornithine decarboxylase levels during recovery.
Conclusions:
- Hyperoxia induces arginase isoforms in the lung in vivo.
- The localization of arginase in connective tissues suggests a role in lung injury and repair, potentially involving fibroblasts.
- Arginase may play a significant role in the lung's response to hyperoxic injury and the subsequent tissue repair processes.