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Am J Physiol Lung Cell Mol Physiol (September 26, 2003). doi:10.1152/ajplung.00326.2002
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Submitted on September 27, 2002
Accepted on September 20, 2003

Downregulation of ENaC Activity and Expression by TNF{alpha} In Alveolar Epithelial Cells

Andre Dagenais1*, Rosalie Frechette1, Yuko Yamagata1, Toshiyuki Yamagata1, Jean-Francois Carmel1, Marie-Eve Clermont1, Emmanuelle Brochiero1, Chantal Masse1, and Yves Berthiaume1

1 Centre de Recherche, Departement de Medecine, Centre Hospitalier de l'Universite de Montreal-Hotel-Dieu, Universite de Montreal, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: andre.dagenais.chum{at}ssss.gouv.qc.ca.

Sodium absorption by an amiloride-sensitive channel is the main driving force of lung liquid clearance at birth and lung edema clearance in adulthood. In this study, we tested if tumor necrosis factor {alpha} (TNF{alpha}) a proinflammatory cytokine involved in several lung pathologies, could modulate sodium absorption in cultured alveolar epithelial cells. We found that TNF{alpha} decreased the expression of the {alpha}, {beta} and {gamma}subunits of epithelial sodium channel (ENaC) mRNA to 36%, 43% and 16% of the controls after 24-h treatment and reduced to 50% the amount of {alpha}ENaC protein in these cells. There was no impact, however, on {alpha}1 and {beta}1 Na+-K+-ATPase mRNA expression. Amiloride-sensitive current and ouabain-sensitive Rb uptake were reduced respectively to 28% and 39% of the controls. A strong correlation was found, at different TNF{alpha} concentrations, between the decrease of amiloride-sensitive current and {alpha}ENaC mRNA expression. All these data show that TNF{alpha}, a proinflammatory cytokine present during lung infection, has a profound influence on the capacity of alveolar epithelial cells to transport sodium.




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