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1 Department of Physiology, Faculté de Médecine Léonard de Vinci, Université Paris 13, 93012 Bobigny cedex, and INSERM Unité 426, Faculté Xavier Bichat, Université Paris 7, 75018 Paris, France; and 2 Cardiovascular Research Institute, University of California, San Francisco, California 94143
Alveolar hypoxia occurs during ascent to
high altitude but is also commonly observed in many acute and chronic
pulmonary disorders. The alveolar epithelium is
directly exposed to decreases in O2 tension, but a few
studies have evaluated the effects of hypoxia on alveolar cell
function. The alveolar epithelium consists of two cell types: large,
flat, squamous alveolar type I and cuboidal type II (ATII). ATII cells
are more numerous and have a number of critical functions, including
transporting ions and substrates required for many physiological
processes. ATII cells express 1) membrane proteins used for
supplying substrates required for cell metabolism and 2) ion
transport proteins such as Na+ channels and
Na+-K+-ATPase, which are involved in the
vectorial transport of Na+ from the alveolar to
interstitial spaces and therefore drive the resorption of alveolar
fluid. This brief review focuses on gene expression regulation of
glucose transporters and Na+ transport proteins by hypoxia
in alveolar epithelial cells. Cells exposed to severe hypoxia (0% or
3% O2) for 24 h upregulate the activity and expression of
the glucose transporter GLUT-1, resulting in preservation of ATP
content. Hypoxia-induced increases in GLUT-1 mRNA levels are due to
O2 deprivation and inhibition of oxidative phosphorylation.
This regulation occurs at the transcriptional level through activation
of a hypoxia-inducible factor. In contrast, hypoxia downregulates
expression and activity of Na+ channels and
Na+-K+-ATPase in cultured alveolar epithelial
cells. Hypoxia induces time- and concentration-dependent decreases of
-, 
-, and 
-subunits of epithelial Na+ channel mRNA
and 1- and 1-subunits of
Na+-K+-ATPase, effects that are completely
reversed after reoxygenation. The mechanisms by which O2
deprivation regulates gene expression of Na+ transport
proteins are not fully elucidated but likely involve the redox status
of the cell. Thus hypoxia regulates gene expression of transport
proteins in cultured alveolar epithelial type II cells differently,
preserving ATP content.
epithelial sodium channel; alveolar epithelial cells; glucose transporters; hypoxia-inducible factor; sodium pump
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