Glucocorticoids regulate nhe-3 transcription in okp cells.
Baum, Michel, Morimasa Amemiya, Vangipuram Dwarakanath, Robert J.
Alpern, and Orson W. Moe.
Departments of Pediatrics and Internal Medicine, University of
Texas Southwestern Medical Center and Department of Veteran Affairs
Medical Center at Dallas, Dallas, Texas
APStracts 2:0128F, 1995.
OKP cells express NHE-3, an amiloride-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 glucocorticoid mediated
increase in Na+/H+ antiporter activity. Incubation of OKP cells with
10-6M dexamethasone resulted in a 2-3 fold increase in NHE-3 mRNA
abundance. This increase was seen after 4 h of incubation with
dexamethasone, a similar time course 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.
Received 18 May 1995; accepted in final form 24 July 1995.
APS Manuscript Number F159-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 August 1995.