Dexamethasone upregulates the Na-K-ATPase in rat alveolar epithelial cells

被引:71
|
作者
Barquin, N
Ciccolella, DE
Ridge, KM
Sznajder, JI
机构
[1] MICHAEL REESE HOSP & MED CTR, CHICAGO, IL 60616 USA
[2] INST NACL ENFERMEDADES RESP, TLALPAN 04000, MEXICO
[3] UNIV ILLINOIS, CHICAGO, IL 60612 USA
关键词
alveolar type II cells; sodium-potassium-adenosinetriphosphatase; regulation of sodium-potassium-adenosinetriphosphatase in lungs;
D O I
10.1152/ajplung.1997.273.4.L825
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 beta(1)-mRNA transcript levels increased in ATII cells 6, 12, and 24 h after dexamethasone exposure (P < 0.05). However, the steady-state alpha(1)-mRNA transcript levels were unchanged. The protein expression for the alpha(1)- and beta(1)-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.
引用
收藏
页码:L825 / L830
页数:6
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