cAMP-stimulated Na+ transport in H441 distal lung epithelial cells: role of PKA, phosphatidylinositol 3-kinase, and sgk1

Am J Physiol Lung Cell Mol Physiol. 2004 Oct;287(4):L843-51. doi: 10.1152/ajplung.00340.2003. Epub 2004 Jun 18.

Abstract

H441 cells, a bronchiolar epithelial cell line, develop a cAMP-regulated benzamil-sensitive Na+ transport pathway on permeable supports (Itani OA, Auerbach SD, Husted RF, Volk KA, Ageloff S, Knepper MA, Stokes JB, Thomas CP. Am J Physiol Lung Cell Mol Physiol 282: L631-L641, 2002). To understand the molecular basis for the stimulation of Na+ transport, we delineated the role of specific intracellular pathways and examined the effect of cAMP on alphabetagamma-epithelial Na+ channel (ENaC) and sgk1 expression. Na+ transport increases within 5 min of cAMP stimulation and is sustained for >24 h. The sustained effect of cAMP on Na+ transport is abolished by LY-294002, an inhibitor of phosphatidylinositol 3-kinase, by H89, an inhibitor of PKA, or by SB-202190, an inhibitor of p38 MAP kinase. The sustained effect of cAMP was associated with increases in alpha-ENaC mRNA and protein but without a detectable increase in betagamma-ENaC and sgk1. The early effect of cAMP on Na+ transport is brefeldin sensitive and is mediated via PKA. These results are consistent with a model where the early effect of cAMP is to increase trafficking of Na+ channels to the apical cell surface whereas the sustained effect requires the synthesis of alpha-ENaC.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Biological Transport / drug effects
  • Cell Line
  • Chromones / pharmacology
  • Colforsin / pharmacology
  • Cyclic AMP / physiology*
  • Cyclic AMP-Dependent Protein Kinases / metabolism*
  • Dexamethasone / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Epithelial Sodium Channels
  • Humans
  • Immediate-Early Proteins
  • Kinetics
  • Lung
  • Morpholines / pharmacology
  • Nuclear Proteins / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Protein Serine-Threonine Kinases / metabolism*
  • Respiratory Mucosa / drug effects
  • Respiratory Mucosa / physiology*
  • Sodium / metabolism*
  • Sodium Channels / physiology
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Chromones
  • Enzyme Inhibitors
  • Epithelial Sodium Channels
  • Immediate-Early Proteins
  • Morpholines
  • Nuclear Proteins
  • Sodium Channels
  • Colforsin
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Dexamethasone
  • Sodium
  • Cyclic AMP
  • Protein Serine-Threonine Kinases
  • serum-glucocorticoid regulated kinase
  • Cyclic AMP-Dependent Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • 1-Methyl-3-isobutylxanthine