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  FXYD1 negatively regulates Na+/K+-ATPase activity in lung alveolar epithelial cells

Wujak, L. A., Blume, A., Baloglu, E., Wygrecka, M., Wygowski, J., Herold, S., et al. (2016). FXYD1 negatively regulates Na+/K+-ATPase activity in lung alveolar epithelial cells. RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY, 220, 54-61. doi:10.1016/j.resp.2015.09.008.

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 Creators:
Wujak, Lukasz A.1, Author              
Blume, Anna, Author
Baloglu, Emel, Author
Wygrecka, Malgorzata, Author
Wygowski, Jegor, Author
Herold, Susanne, Author
Mayer, Konstantin, Author
Vadasz, Istvan, Author
Besuch, Petra, Author
Mairbaeurl, Heimo, Author
Seeger, Werner1, Author              
Morty, Rory E.1, Author              
Affiliations:
1Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591698              

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Free keywords: RESPIRATORY-DISTRESS-SYNDROME; GROWTH-FACTOR-BETA; ADENOVIRUS-MEDIATED TRANSFER; NA-K-ATPASE; PULMONARY-EDEMA; FLUID CLEARANCE; TRANSFORMING GROWTH-FACTOR-BETA-1; LIQUID CLEARANCE; DECREASES EXPRESSION; ION-TRANSPORTPhysiology; Respiratory System; ARDS; TGF-beta; Na+/K+-ATPase; FXYD; Ion transport; Edema;
 Abstract: Acute respiratory distress syndrome CARDS) is clinical syndrome characterized by decreased lung fluid reabsorption, causing alveolar edema. Defective alveolar ion transport undertaken in part by the Na+/K+-ATPase underlies this compromised fluid balance, although the molecular mechanisms at play are not understood. We describe here increased expression of FXYD1, FXYD3 and FXYD5, three regulatory subunits of the Na+/K+-ATPase, in the lungs of ARDS patients. Transforming growth factor (TGF)-beta, a pathogenic mediator of ARDS, drove increased FXYD1 expression in A549 human lung alveolar epithelial cells, suggesting that pathogenic TGF-beta signaling altered Na+/K+-ATPase activity in affected lungs. Lentivirus-mediated delivery of FXYD1 and FXYD3 allowed for overexpression of both regulatory subunits in polarized H441 cell monolayers on an air/liquid interface. FXYD1 but not FXYD3 overexpression inhibited amphotericin B-sensitive equivalent short-circuit current in Ussing chamber studies. Thus, we speculate that FXYD1 overexpression in ARDS patient lungs may limit Na+/K+-ATPase activity, and contribute to edema persistence. (C) 2015 Elsevier B.V. All rights reserved.

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Language(s): eng - English
 Dates: 2016
 Publication Status: Published in print
 Pages: 8
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Degree: -

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Title: RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Source Genre: Journal
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Publ. Info: PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS : ELSEVIER SCIENCE BV
Pages: - Volume / Issue: 220 Sequence Number: - Start / End Page: 54 - 61 Identifier: ISSN: 1569-9048