Corpus ID: 24278865

Hypoxia and beta 2-agonists regulate cell surface expression of the epithelial sodium channel in native alveolar epithelial cells.

  title={Hypoxia and beta 2-agonists regulate cell surface expression of the epithelial sodium channel in native alveolar epithelial cells.},
  author={Carole Plan{\`e}s and Marcel Blot-Chabaud and Michael A. Matthay and Sylviane Couette and Tokujiro Uchida and Christine Cl{\'e}rici},
  journal={The Journal of biological chemistry},
  volume={277 49},
Alveolar hypoxia may impair sodium-dependent alveolar fluid transport and induce pulmonary edema in rat and human lung, an effect that can be prevented by the inhalation of beta(2)-agonists. To investigate the mechanism of beta(2)-agonist-mediated stimulation of sodium transport under conditions of moderate hypoxia, we examined the effect of terbutaline on epithelial sodium channel (ENaC) expression and activity in cultured rat alveolar epithelial type II cells exposed to 3% O(2) for 24 h… Expand
The role of hypoxia-induced modulation of alveolar epithelial Na+- transport in hypoxemia at high altitude
Results indicate that a HIF-2α-dependent decrease in Na+-transport in hypoxic alveolar epithelium decreases alveolars reabsorption, which might further enhance hypoxic pulmonary vasoconstriction and cause HAPE. Expand
β 2-Adrenergic Stimulation Blunts Inhibition of Epithelial Ion Transport by Hypoxia of Rat Alveolar Epithelial Cells
Results indicate that β 2 adrenergic stimulation increased Na+- and Cl- transport in ATII cells even in hypoxia thus restoring normal reabsorption, and acute and prolonged treatment with terbutaline prevented hypoxic inhibition of ion transport. Expand
Dexamethasone prevents transport inhibition by hypoxia in rat lung and alveolar epithelial cells by stimulating activity and expression of Na+-K+-ATPase and epithelial Na+ channels.
It is indicated that DEX prevents inhibition of alveolar reabsorption by hypoxia and stimulates the expression of Na transporters even when it is applied in Hypoxia. Expand
In vitro hypoxia impairs beta2-adrenergic receptor signaling in primary rat alveolar epithelial cells.
Results indicate that despite the decrease in G(s) protein level G( s) protein was still functional and that hypoxia impairs beta(2)-AR signaling due to an increased activity of G(i/o) proteins. Expand
Epithelial Sodium Channels in the Adult Lung – Important Modulators of Pulmonary Health and Disease
βadrenergic agonists have been shown experimentally to reverse defects in ENaC function, and improve hypoxemia and pulmonary edema, and may provide a novel therapeutic modality for ARDS, although some viral lung pathogens appear to induce insensitivity to their actions. Expand
Role of the small GTPase RhoA in the hypoxia-induced decrease of plasma membrane Na,K-ATPase in A549 cells
Evidence is provided that in human alveolar epithelial cells exposed to hypoxia, RhoA/ROCK activation is necessary for Na,K-ATPase endocytosis via a mechanism that requires mitochondrial ROS. Expand
AMP-activated protein kinase regulates CO2-induced alveolar epithelial dysfunction in rats and human cells by promoting Na,K-ATPase endocytosis.
Evidence is provided that elevated CO(2) levels are sensed by AECs and that AMPK mediatesCO(2)-induced Na,K-ATPase endocytosis and alveolar epithelial dysfunction, which can be prevented with beta-adrenergic agonists and cAMP. Expand
Hypoxia-induced cytoskeleton disruption in alveolar epithelial cells.
Hypoxia disrupted cytoskeleton and TJ organization in AEC and may participate, at least in part, to hypoxia-induced decrease in Na transport, which is indicated to affect ion and fluid transport. Expand
Conditioned media from mesenchymal stromal cells restore sodium transport and preserve epithelial permeability in an in vitro model of acute alveolar injury.
Results indicate that MSC-M may be a preferable therapeutic option for ALI, and suggest a possible role for KGF in the beneficial effect of M SCs. Expand
Loss of barrier integrity in alveolar epithelial cells downregulates ENaC expression and activity via Ca2+ and TRPV4 activation
The results suggest that mechanical stress induced by wounding or TRPV4-mediated loss of tight junction increases [Ca2+]i and elicits a Ca2+ wave that affects ENaC expression and function away from the site of injury. Expand