Dexamethasone responsive element in the rat Na, K-ATPase β 1 gene coding region

Hong Hao, Richard Rhodes, David H. Ingbar, Christine H. Wendt

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

The Na, K-ATPase plays an essential role in active alveolar epithelial fluid resorption. In fetal and adult alveolar epithelial cells, glucocorticoids (GC) increase Na, K-ATPase activity, mRNA levels, and transcription rate of the β1 subunit. In this study, we describe a glucocorticoid responsive element (GRE) in the coding region of the rat Na, K-ATPase β1 gene in a rat lung epithelial cell line. Transient transfection experiments with the β1 subunit coding region with or without the 5′ and 3′ untranslated regions demonstrated responsiveness to dexamethasone induction and also identified a GRE at +434 in exon IV. The +434 GRE conferred dexamethasone responsiveness in a heterologous thymidine kinase promoter irrespective of its orientation to the β 1 promoter. Transcriptional upregulation by dexamethasone was abolished in +434 mutants. Electrophoretic mobility shift assays (EMSA) demonstrated specific binding of nuclear proteins to the +434 GRE and the presence of the GC receptor. This specific binding was inhibited by a GRE previously described in the rat Na, K-ATPase β1 gene at -631. In conclusion, we identified a GRE at +434 in the exon IV of the rat Na, K-ATPase β1 gene.

Original languageEnglish (US)
Pages (from-to)55-63
Number of pages9
JournalBiochimica et Biophysica Acta - Gene Structure and Expression
Volume1630
Issue number2-3
DOIs
StatePublished - Nov 30 2003

Keywords

  • Enhancer
  • Gene regulation
  • Glucocorticoid receptor
  • Glucocorticoid response element
  • Ion transport
  • Sodium pump

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