Glucocorticoids regulate NHE-3 transcription in OKP cells

Michel Baum, Morimasa Amemiya, Vangipuram Dwarakanath, Robert J. Alpern, Orson W. Moe

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

OKP cells express NHE-3. an amilo-ride-resistant Na+/H+ antiporter, which is likely an isoform responsible for apical proton secretion by the proximal tubule. We have previously shown that an amiloride-resistant Na+/H+ antiporter in OKP cells is regulated by dexamethasone, a synthetic glucocorticoid. The purpose of the present study was to examine the mechanism for the glucocorticoidmediated increase in Na+/H+ antiporter activity. Incubation of OKP cells with 10-6 M dexamethasone resulted in a two- to threefold increase in NHE-3 mRNA abundance. This increase was seen after 4 h of incubation with dexamethasone, a time course similar to that found for Na+/H+ antiporter activity. To examine the mechanism for the increase in NHE-3 mRNA abundance, mRNA half-life and in vitro transcription experiments were performed. NHE-3 mRNA had a half-life of 8 h in control and dexamethasone-treated cells. The rate of in vitro transcription was 1.8-fold greater when OKP cells were treated with dexamethasone. These data suggest that the glucocorticoid-mediated increase in Na+/H+ antiporter activity is due to an increase in NHE-3 gene transcription.

Original languageEnglish (US)
Pages (from-to)F164-F169
JournalAmerican Journal of Physiology
Volume270
Issue number1 PART 2
StatePublished - Dec 1 1996

Keywords

  • Dexamethasone
  • Proximal tubule
  • Sodium/proton exchanger

ASJC Scopus subject areas

  • Physiology (medical)

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    Baum, M., Amemiya, M., Dwarakanath, V., Alpern, R. J., & Moe, O. W. (1996). Glucocorticoids regulate NHE-3 transcription in OKP cells. American Journal of Physiology, 270(1 PART 2), F164-F169.