ArticleThe Biochemical journal2009
Glucocorticoids can activate the alpha-ENaC gene promoter independently of SGK1.
Article in The Biochemical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Optimizing the use of in vitro transcribed SGK1-mRNA as a therapeutic tool to treat female infertility.BMC research notes · 2025Article
- Sex differences in airway disease: estrogen and airway surface liquid dynamics.Biology of sex differences · 2024Review
- Glucocorticoids, sodium transport mediators, and respiratory distress syndrome in preterm infants.Pediatric research · 2021Article
- Regulation of Lung Epithelial Sodium Channels by Cytokines and Chemokines.Frontiers in immunology · 2017Review
- Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis.International journal of molecular sciences · 2016Review
- Dexamethasone and insulin activate serum and glucocorticoid-inducible kinase 1 (SGK1) via different molecular mechanisms in cortical collecting duct cells.Physiological reports · 2016Article
- Systemic steroid exposure is associated with differential methylation in chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2012Article
- Epithelial Na⁺ channel activity in human airway epithelial cells: the role of serum and glucocorticoid-inducible kinase 1.British journal of pharmacology · 2012Article
- Dexamethasone-induced up-regulation of two-pore domain K+ channel genes, TASK-1 and TWIK-2, in cultured human periodontal ligament fibroblasts.In vitro cellular & developmental biology. Animal · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The role of SGK1 (serum- and glucocorticoid-induced protein kinase 1) in the glucocorticoid induction of alpha-ENaC (epithelial Na+ channel alpha subunit) gene transcription was explored by monitoring the transcriptional activity of a luciferase-linked, alpha-ENaC reporter gene construct (pGL3-KR1) expressed in H441 airway epithelial cells. Dexamethasone evoked a concentration-dependent (EC50 approximately 4 microM) increase in transcriptional activity dependent upon a glucocorticoid response element in the alpha-ENaC sequence. Although dexamethasone also activated endogenous SGK1, artificially increasing cellular SGK1 activity by expressing a constitutively active SGK1 mutant (SGK1-S422D) in hormone-deprived cells did not activate pGL3-KR1. Moreover, expression of catalytically inactive SGK1 (SGK1-K127A) suppressed the activation of endogenous SGK1 without affecting the transcriptional response to dexamethasone. Increasing cellular PI3K (phosphoinositide 3-kinase) activity by expressing a membrane-anchored form of the catalytic PI3K-P110alpha subunit [CD2 (cluster of differentiation 2)-P110alpha] also activated endogenous SGK1 without affecting pGL3-KR1activity. A catalytically inactive form of CD2-P110alpha (R1130P), on the other hand, prevented the dexamethasone-induced activation of SGK1, but did not inhibit the activation of pGL3-KR1. However, expression of SGK1-S422D or CD2-P110alpha enhanced the transcriptional responses to maximally effective concentrations of dexamethasone and this effect occurred with no change in EC50. Dexamethasone-induced (0.3-300 nM) activation of pGL3-KR1 was unaffected by inhibitors of PI3K (PI-103 and wortmanin) and by rapamycin, a selective inhibitor of the TORC1 (target of rapamycin complex 1) signalling complex. Dexamethasone-induced activation of the alpha-ENaC gene promoter can thus occur independently of SGK1/PI3K, although this pathway does provide a mechanism that allows this transcriptional response to dexamethasone to be enhanced.
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