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Hyperoxia Upregulated Na,K-Adenosine Triphosphatase β1 Gene Transcription*

Christine H. Wendt, MD, FCCP; Renuka Sharma, MS; Howard Towle, PhD; Gregory Gick, PhD; David H. Ingbar, MD, FCCP
Author and Funding Information

*From the University of Minnesota Medical School (Drs. Wendt, Towle, and Ingbar, and Ms. Sharma), Minneapolis, MN; and State University of New York (Dr. Gick), Brooklyn, NY.

Correspondence to: Christine H. Wendt, MD, FCCP, Assistant Professor of Medicine, Pulmonary and Critical Care, University of Minnesota, FUMC Box 276, 420 Delaware St SE, Minneapolis, MN 55455; e-mail: wendt005@gold.tc.umn.edu



Chest. 1999;116(suppl_1):87S-88S. doi:10.1378/chest.116.suppl_1.87S
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Extract

Alveolar sodium and fluid transport occur via type II cell apical sodium channels and basolateral Na,K-adenosine triphosphatases (ATPases), both of which are fundamental in resorbing edema fluid and restoring gas exchange following lung injury.1 Na,K-ATPase gene expression is upregulated in the whole lung and type II cells in both in vitro and in vivo models of hyperoxic lung injury.5 This increase in Na,K-ATPase may serve as an homeostatic protective mechanism against alveolar flooding. Using a type II cell in vitro model of hyperoxic injury (≥ 95% O2 for 48 h), we demonstrated a threefold and fivefold increase in steady-state levels of Na,K-ATPase α1 and β1 subunit messenger RNA (mRNA), respectively.,23,6 In addition, hyperoxia did not alter messenger RNA stability of either subunit.7 To study the mechanism of Na,K-ATPase gene upregulation by hyperoxia, we developed an in vitro model using MDCK cells exposed to hyperoxia (95% O2/5% CO2 for 24 to 48 h).,7


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