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Glucocorticoid-stimulated lung epithelial Na(+) transport is associated with regulated ENaC and sgk1 expression.
Am J Physiol Lung Cell Mol Physiol. 2002 Apr; 282(4):L631-41.AJ

Abstract

H441 cells, a bronchiolar epithelial cell line, develop a glucocorticoid-regulated amiloride-sensitive Na(+) transport pathway on permeable supports (R. Sayegh, S. D. Auerbach, X. Li, R. Loftus, R. Husted, J. B. Stokes, and C. P. Thomas. J Biol Chem 274: 12431-12437, 1999). To understand its molecular basis, we examined the effect of glucocorticoids (GC) on epithelial Na(+) channel (ENaC)-alpha, -beta, and -gamma and sgk1 expression and determined the biophysical properties of Na(+) channels in these cells. GC stimulated the expression of ENac-alpha, -beta, and -gamma and sgk1 mRNA, with the first effect seen by 1 h. These effects were abolished by actinomycin D, but not by cycloheximide, indicating a direct stimulatory effect on ENaC and sgk1 mRNA synthesis. The GC effect on transcription of ENaC-alpha mRNA was accompanied by a significant increase in ENaC-alpha protein levels. GC also stimulated ENaC-alpha, -beta, and -gamma and sgk1 mRNA expression in A549 cells, an alveolar type II cell line. To determine the biophysical properties of the Na(+) channel, single-channel currents were recorded from cell-attached H441 membranes. An Na(+)-selective channel with slow kinetics and a slope conductance of 10.8 pS was noted, properties similar to ENaC-alpha, -beta, and -gamma expressed in Xenopus laevis oocytes. These experiments indicate that amiloride-sensitive Na(+) transport is mediated through classic ENaC channels in human lung epithelia and that GC-regulated Na(+) transport is accompanied by increased transcription of each of the component subunits and sgk1.

Authors+Show Affiliations

Department of Internal Medicine, University of Iowa College of Medicine, 200 Hawkins Drive, Iowa City, IA 52242, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
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.

Language

eng

PubMed ID

11880287

Citation

Itani, Omar A., et al. "Glucocorticoid-stimulated Lung Epithelial Na(+) Transport Is Associated With Regulated ENaC and Sgk1 Expression." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 282, no. 4, 2002, pp. L631-41.
Itani OA, Auerbach SD, Husted RF, et al. Glucocorticoid-stimulated lung epithelial Na(+) transport is associated with regulated ENaC and sgk1 expression. Am J Physiol Lung Cell Mol Physiol. 2002;282(4):L631-41.
Itani, O. A., Auerbach, S. D., Husted, R. F., Volk, K. A., Ageloff, S., Knepper, M. A., Stokes, J. B., & Thomas, C. P. (2002). Glucocorticoid-stimulated lung epithelial Na(+) transport is associated with regulated ENaC and sgk1 expression. American Journal of Physiology. Lung Cellular and Molecular Physiology, 282(4), L631-41.
Itani OA, et al. Glucocorticoid-stimulated Lung Epithelial Na(+) Transport Is Associated With Regulated ENaC and Sgk1 Expression. Am J Physiol Lung Cell Mol Physiol. 2002;282(4):L631-41. PubMed PMID: 11880287.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucocorticoid-stimulated lung epithelial Na(+) transport is associated with regulated ENaC and sgk1 expression. AU - Itani,Omar A, AU - Auerbach,Scott D, AU - Husted,Russell F, AU - Volk,Kenneth A, AU - Ageloff,Shana, AU - Knepper,Mark A, AU - Stokes,John B, AU - Thomas,Christie P, PY - 2002/3/7/pubmed PY - 2002/4/12/medline PY - 2002/3/7/entrez SP - L631 EP - 41 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am J Physiol Lung Cell Mol Physiol VL - 282 IS - 4 N2 - H441 cells, a bronchiolar epithelial cell line, develop a glucocorticoid-regulated amiloride-sensitive Na(+) transport pathway on permeable supports (R. Sayegh, S. D. Auerbach, X. Li, R. Loftus, R. Husted, J. B. Stokes, and C. P. Thomas. J Biol Chem 274: 12431-12437, 1999). To understand its molecular basis, we examined the effect of glucocorticoids (GC) on epithelial Na(+) channel (ENaC)-alpha, -beta, and -gamma and sgk1 expression and determined the biophysical properties of Na(+) channels in these cells. GC stimulated the expression of ENac-alpha, -beta, and -gamma and sgk1 mRNA, with the first effect seen by 1 h. These effects were abolished by actinomycin D, but not by cycloheximide, indicating a direct stimulatory effect on ENaC and sgk1 mRNA synthesis. The GC effect on transcription of ENaC-alpha mRNA was accompanied by a significant increase in ENaC-alpha protein levels. GC also stimulated ENaC-alpha, -beta, and -gamma and sgk1 mRNA expression in A549 cells, an alveolar type II cell line. To determine the biophysical properties of the Na(+) channel, single-channel currents were recorded from cell-attached H441 membranes. An Na(+)-selective channel with slow kinetics and a slope conductance of 10.8 pS was noted, properties similar to ENaC-alpha, -beta, and -gamma expressed in Xenopus laevis oocytes. These experiments indicate that amiloride-sensitive Na(+) transport is mediated through classic ENaC channels in human lung epithelia and that GC-regulated Na(+) transport is accompanied by increased transcription of each of the component subunits and sgk1. SN - 1040-0605 UR - https://www.unboundmedicine.com/medline/citation/11880287/Glucocorticoid_stimulated_lung_epithelial_Na_+__transport_is_associated_with_regulated_ENaC_and_sgk1_expression_ L2 - https://journals.physiology.org/doi/10.1152/ajplung.00085.2001?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -