Insulin regulates alveolar epithelial function by inducing Na +/K+-ATPase translocation to the plasma membrane in a process mediated by the action of Akt

Alejandro P. Comellas, Aileen M. Kelly, Humberto E. Trejo, Arturo Briva, Joyce Lee, Jacob I. Sznajder, Laura A. Dada

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Stimulation of Na+/K+-ATPase translocation to the cell surface increases active Na+ transport, which is the driving force of alveolar fluid reabsorption, a process necessary to keep the lungs free of edema and to allow normal gas exchange. Here, we provide evidence that insulin increases alveolar fluid reabsorption and Na+/K +-ATPase activity by increasing its translocation to the plasma membrane in alveolar epithelial cells. Insulin-induced Akt activation is necessary and sufficient to promote Na+/K+-ATPase translocation to the plasma membrane. Phosphorylation of AS160 by Akt is also required in this process, whereas inactivation of the Rab GTPase-activating protein domain of AS160 promotes partial Na+/K+-ATPase translocation in the absence of insulin. We found that Rab10 functions as a downstream target of AS160 in insulin-induced Na+/K +-ATPase translocation. Collectively, these results suggest that Akt plays a major role in Na+/K+-ATPase intracellular translocation and thus in alveolar fluid reabsorption.

Original languageEnglish (US)
Pages (from-to)1343-1351
Number of pages9
JournalJournal of cell science
Volume123
Issue number8
DOIs
StatePublished - Apr 15 2010

Keywords

  • Akt
  • Alveolar epithelium
  • Na/K-ATPase

ASJC Scopus subject areas

  • Cell Biology

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