Affiliation:
1. Pulmonary and Critical Care Medicine, Michael Reese Hospital and Medical Center, Chicago 60616; University of Illinois at Chicago, Chicago, Illinois 60612; and Instituto Nacional de Enfermedades Respiratorias, Tlalpan, Mexico 04000
Abstract
Previous studies in kidney, heart, and liver cells have demonstrated that dexamethasone regulates the expression of Na-K-ATPase. In the lungs, Na-K-ATPase has been reported in alveolar epithelial type II (ATII) cells and is thought to participate in active Na+ transport and lung edema clearance. The aim of this study was to determine whether Na-K-ATPase would be regulated by dexamethasone in cultured rat ATII cells. Regulation of the Na-K-ATPase by dexamethasone could lead to a greater understanding of its role in active Na+ transport and lung edema clearance. Rat ATII cells were isolated, plated for 24 h, and exposed to 10−7 and 10−8 M dexamethasone. These cells were harvested at 0, 3, 6, 12, and 24 h after dexamethasone exposure for determination of steady-state Na-K-ATPase mRNA transcript levels, protein expression, and function. The steady-state Na-K-ATPase β1-mRNA transcript levels increased in ATII cells 6, 12, and 24 h after dexamethasone exposure ( P < 0.05). However, the steady-state α1-mRNA transcript levels were unchanged. The protein expression for the α1- and β1-subunits increased in ATII cells exposed to dexamethasone compared with controls in association with a temporal increase in Na-K-ATPase function after dexamethasone exposure. These results suggest that dexamethasone regulates Na-K-ATPase in ATII cells possibly by transcriptional, translational, and posttranslational mechanisms.
Publisher
American Physiological Society
Subject
Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology
Cited by
66 articles.
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