Main |
Browse Volumes |
Forthcoming Volumes |
Annals PrePrints |
Annals Extra |
E-mail Alerts |
Subscriptions & Orders |
New Proposals |
Author Guidelines |
About Annals |
Help |
 |
|
|
|
|
|
Alveolar Cell Death in Hyperoxia-Induced Lung Injury
ALESSANDRA PAGANO AND
CONSTANCE BARAZZONE-ARGIROFFO
Departments of Pediatrics and Pathology, University of Geneva Medical School, Geneva, Switzerland
Address for correspondence: Dr. Constance Barazzone Argiroffo, Department of Pathology and Department of Pediatrics, Centre Médical Universitaire, 1211 Geneva 4, Switzerland. Voice: +41 22 702 57 57; fax: +41 22 702 57 46. constance.barazzone{at}hcuge.ch
Ann. N.Y. Acad. Sci. 1010: 405-416 (2003).
Exposure to high oxygen concentration causes direct oxidative cell damage through increased production of reactive oxygen species. In vivo oxygen-induced lung injury is well characterized in rodents and has been used as a valuable model of human respiratory distress syndrome. Hyperoxia-induced lung injury can be considered as a bimodal process resulting (1) from direct oxygen toxicity and (2) from the accumulation of inflammatory mediators within the lungs. Both apoptosis and necrosis have been described in alveolar cells (mainly epithelial and endothelial) during hyperoxia. While the in vitro response to oxygen seems to be cell type-dependent in tissue cultures, it is still unclear which are the death mechanisms and pathways implicated in vivo. Even though it is not yet possible to distinguish unequivocally between apo-ptosis, necrosis, or other intermediate form(s) of cell death, a great variety of strategies has been shown to prevent alveolar damage and to increase animal survival during hyperoxia. In this review, we summarize the different cell death pathways leading to alveolar damage during hyperoxia, with particular attention to the pivotal role of mitochondria. In addition, we discuss the different protective mechanisms potentially interfering with alveolar cell death.
Key Words: hyperoxia • lung • mice • apoptosis • necrosis • mitochondria
This article has been cited by other articles:
|
|
|
|
 
L. S. Prince
Hyperoxia and EGFL7: saving cells from too much of a good thing
Am J Physiol Lung Cell Mol Physiol,
January 1, 2008;
294(1):
L15 - L16.
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. E. Tipple, S. E. Welty, L. K. Rogers, T. N. Hansen, Y.-E. Choi, J. P. Kehrer, and C. V. Smith
Thioredoxin-Related Mechanisms in Hyperoxic Lung Injury in Mice
Am. J. Respir. Cell Mol. Biol.,
October 1, 2007;
37(4):
405 - 413.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Irwin, K. Helm, N. Campbell, M. Imamura, K. Fagan, J. Harral, M. Carr, K. A. Young, D. Klemm, S. Gebb, et al.
Neonatal lung side population cells demonstrate endothelial potential and are altered in response to hyperoxia-induced lung simplification
Am J Physiol Lung Cell Mol Physiol,
October 1, 2007;
293(4):
L941 - L951.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Choo-Wing, J. H. Nedrelow, R. J. Homer, J. A. Elias, and V. Bhandari
Developmental differences in the responses of IL-6 and IL-13 transgenic mice exposed to hyperoxia
Am J Physiol Lung Cell Mol Physiol,
July 1, 2007;
293(1):
L142 - L150.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Xu, J. R. Guthrie, S. Mabry, T. M. Sack, and W. E. Truog
Mitochondrial aldehyde dehydrogenase attenuates hyperoxia-induced cell death through activation of ERK/MAPK and PI3K-Akt pathways in lung epithelial cells
Am J Physiol Lung Cell Mol Physiol,
November 1, 2006;
291(5):
L966 - L975.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. McAdams, S. B. Mustafa, J. S. Shenberger, P. S. Dixon, B. M. Henson, and R. J. DiGeronimo
Cyclic stretch attenuates effects of hyperoxia on cell proliferation and viability in human alveolar epithelial cells
Am J Physiol Lung Cell Mol Physiol,
August 1, 2006;
291(2):
L166 - L174.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Lee, R. Reddy, L. Barsky, K. Weinberg, and B. Driscoll
Contribution of proliferation and DNA damage repair to alveolar epithelial type 2 cell recovery from hyperoxia
Am J Physiol Lung Cell Mol Physiol,
April 1, 2006;
290(4):
L685 - L694.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
