help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Published ahead of print on June 1, 2006, doi:10.1165/rcmb.2005-0478OC

Am. J. Respir. Cell Mol. Biol., Volume 35, Number 5, November 2006, 519-527

A more recent version of this article appeared on November 1, 2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2005-0478OCv1
35/5/519    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bouvry, D.
Right arrow Articles by Clerici, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bouvry, D.
Right arrow Articles by Clerici, C.

Submitted on December 23, 2005
Revised on June 1, 2006

Hypoxia-induced Cytoskeleton Disruption in Alveolar Epithelial Cells

Diane Bouvry1, Carole Planes1, Laurence Malbert-Colas1, Virginie Escabasse1, and Christine Clerici1*

1 Service de Physiologie, INSERM U773 Centre de Recherche Biomedicale Bichat-Beaujon (CRB3); Universite Paris 7 - Denis Diderot, UFR de Medecine; AP HP Hopital Bichat, paris cedex 18, France

* To whom correspondence should be addressed. E-mail: christine.clerici{at}bch.aphp.fr.

Alveolar hypoxia, a common feature of many respiratory disorders, has been previously reported to induce functional changes, particularly a decrease of transepithelial Na and fluid transport. In polarized epithelia, cytoskeleton plays a regulatory role in transcellular and paracellular transport of ions and fluid. We hypothesized that exposure to hypoxia could damage cytoskeleton organization, which in turn, may adversely affect ion and fluid transport. Primary rat alveolar epithelial cells (AEC) were exposed to either mild (3% O2) or severe (0.5% O2) hypoxia for 18 hours or normoxia (21% O2). First, mild and severe hypoxia induced a disorganization of actin, a major protein of the cytoskeleton, reflected by disruption of F-actin filaments. Second, {alpha}-spectrin, an apical cytoskeleton protein, which binds to actin cytoskeleton and Na transport proteins, was cleaved by hypoxia. Pre-treatment of AEC by acaspase inhibitor (z-VAD-fmk; 90µM) blunted hypoxia-induced spectrin cleavage as well as hypoxia-induced decrease in surface membrane {alpha}-EnaC and concomitantly induced a partial recovery of hypoxia-induced decrease of amiloride-sensitive Na transport at 3% O2. Finally, tight junctions (TJs) proteins, which are linked to actin and are a determinant of paracellular permeability, were altered by mild and severe hypoxia: hypoxia induced a mislocalization of occludin from the TJ to cytoplasm and a decrease in zonula occludens-1 protein (ZO-1) level. These modifications were associated with modest changes in paracellular permeability at 0% O2, as assessed by small 4 kD dextran flux and transepithelial resistance measurements. Taken together, these findings indicate that hypoxia disrupted cytoskeleton and TJ organization in alveolar epithelial cells and may participate, at least in part, to hypoxia-induced decrease in Na transport.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. Mitrovic, A. Dymowska, G. E. Nilsson, and S. F. Perry
Physiological consequences of gill remodeling in goldfish (Carassius auratus) during exposure to long-term hypoxia
Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2009; 297(1): R224 - R234.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. Baloglu, A. Ke, I. H. Abu-Taha, P. Bartsch, and H. Mairbaurl
In vitro hypoxia impairs {beta}2-adrenergic receptor signaling in primary rat alveolar epithelial cells
Am J Physiol Lung Cell Mol Physiol, March 1, 2009; 296(3): L500 - L509.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. Clerici and C. Planes
Gene regulation in the adaptive process to hypoxia in lung epithelial cells
Am J Physiol Lung Cell Mol Physiol, March 1, 2009; 296(3): L267 - L274.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
M. M. Berger, C. S. Rozendal, C. Schieber, M. Dehler, S. Zugel, H. J. Bardenheuer, P. Bartsch, and H. Mairbaurl
The Effect of Endothelin-1 on Alveolar Fluid Clearance and Pulmonary Edema Formation in the Rat
Anesth. Analg., January 1, 2009; 108(1): 225 - 231.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
S. Teranishi, K. Kimura, K. Kawamoto, and T. Nishida
Protection of Human Corneal Epithelial Cells from Hypoxia-Induced Disruption of Barrier Function by Keratinocyte Growth Factor
Invest. Ophthalmol. Vis. Sci., June 1, 2008; 49(6): 2432 - 2437.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
P. Rosenberger, J. Khoury, T. Kong, T. Weissmuller, A. M. Robinson, and S. P. Colgan
Identification of vasodilator-stimulated phosphoprotein (VASP) as an HIF-regulated tissue permeability factor during hypoxia
FASEB J, August 1, 2007; 21(10): 2613 - 2621.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2006 American Thoracic Society. 		  ATS Coding and Billing Quarterly