AJP - Lung Columbus Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (August 12, 2005). doi:10.1152/ajplung.00133.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
290/1/L32    most recent
00133.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Auten, R. L
Right arrow Articles by Whorton, M. H
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Auten, R. L
Right arrow Articles by Whorton, M. H
Submitted on March 23, 2005
Accepted on August 8, 2005

TRANSGENIC EXTRACELLULAR SUPEROXIDE DISMUTASE (EC-SOD) PROTECTS POST-NATAL ALVEOLAR EPITHELIAL PROLIFERATION AND DEVELOPMENT DURING HYPEROXIA

Richard L Auten1*, Michael A O'Reilly2, Tim D Oury3, Eva Nozik-Grayck4, and Mary H Whorton4

1 Department of Pediatrics, Duke University Medical Center, Durham, NC, USA; Department of Cell Biology, Duke University Medical Center, Durham, NC, USA
2 Department of Pediatrics, University of Rochester, Rochester, NY, USA; Environmental Medicine, University of Rochester, Rochester, NY, USA
3 Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA
4 Department of Pediatrics, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: auten{at}duke.edu.

Transgenic (TG) human (h) EC-SOD targeted to type II cells protects post-natal newborn mouse lung development against hyperoxia by unknown mechanisms. Since alveolar development depends on timely proliferation of type II epithelium and differentiation to type I epithelium, we measured proliferation in bronchiolar and alveolar (SP-C positive) epithelium in air and 95%O2-exposed wild-type (WT) and TG-hEC-SOD newborn mice at post-natal (P) days 3, 5, and 7, traversing the transition from saccular to alveolar stages. We found that TG hEC-SOD ameliorated the 95%O2-impaired BrdU uptake in alveolar and bronchiolar epithelium at P3, but not at P5 and P7 when overall epithelial proliferation rates were lower in air-exposed WT mice. Mouse EC-, CuZn- and Mn-SOD expression were unaffected by hyperoxia or genotype. TG mice had less DNA damage than 95%O2-exposed WT mice at P3, measured by terminal transferase nick-end labeling (TUNEL), p<.05. Hyperoxia induced cell-cycle inhibitory protein p21cip/waf mRNA at P3, WT > TG, p=.06. 95%O2 impaired apical expression of type I cell {alpha} protein (T1{alpha}, in WT but not in TG mice at P3 and increased T1{alpha} in WT and TG mice at P7. Reducing the 95%O2-induced impairment of epithelial proliferation at a critical window of lung development was associated with protection against DNA damage and preservation of apical T1{alpha} expression at P3.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
M. Yee, P. R. Chess, S. A. McGrath-Morrow, Z. Wang, R. Gelein, R. Zhou, D. A. Dean, R. H. Notter, and M. A. O'Reilly
Neonatal oxygen adversely affects lung function in adult mice without altering surfactant composition or activity
Am J Physiol Lung Cell Mol Physiol, October 1, 2009; 297(4): L641 - L649.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
R. L. Auten, S. N. Mason, K. M. Auten, and M. Brahmajothi
Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice
Am J Physiol Lung Cell Mol Physiol, July 1, 2009; 297(1): L134 - L142.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
K. Ganguly, M. Depner, C. Fattman, K. Bein, T. D. Oury, S. C. Wesselkamper, M. T. Borchers, M. Schreiber, F. Gao, E. von Mutius, et al.
Superoxide dismutase 3, extracellular (SOD3) variants and lung function
Physiol Genomics, May 13, 2009; 37(3): 260 - 267.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. Nozik-Grayck, H. B. Suliman, S. Majka, J. Albietz, Z. Van Rheen, K. Roush, and K. R. Stenmark
Lung EC-SOD overexpression attenuates hypoxic induction of Egr-1 and chronic hypoxic pulmonary vascular remodeling
Am J Physiol Lung Cell Mol Physiol, September 1, 2008; 295(3): L422 - L430.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
O. M. Granillo, M. V. Brahmajothi, S. Li, A. R. Whorton, S. N. Mason, T. J. McMahon, and R. L. Auten
Pulmonary alveolar epithelial uptake of S-nitrosothiols is regulated by L-type amino acid transporter
Am J Physiol Lung Cell Mol Physiol, July 1, 2008; 295(1): L38 - L43.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
F. Kamezaki, H. Tasaki, K. Yamashita, M. Tsutsui, S. Koide, S. Nakata, A. Tanimoto, M. Okazaki, Y. Sasaguri, T. Adachi, et al.
Gene Transfer of Extracellular Superoxide Dismutase Ameliorates Pulmonary Hypertension in Rats
Am. J. Respir. Crit. Care Med., January 15, 2008; 177(2): 219 - 226.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
R. L. Auten, S. N. Mason, M. H. Whorton, W. R. Lampe, W. M. Foster, R. N. Goldberg, B. Li, J. S. Stamler, and K. M. Auten
Inhaled Ethyl Nitrite Prevents Hyperoxia-impaired Postnatal Alveolar Development in Newborn Rats
Am. J. Respir. Crit. Care Med., August 1, 2007; 176(3): 291 - 299.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
P. Yang, J. J. Peairs, R. Tano, and G. J. Jaffe
Oxidant-mediated Akt Activation in Human RPE Cells.
Invest. Ophthalmol. Vis. Sci., October 1, 2006; 47(10): 4598 - 4606.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.