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Glucocorticoids regulate NHE-3 transcription in OKP cells
M Baum1, M Amemiya, V Dwarakanath
1Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, USA.
The American Journal of Physiology
|January 1, 1996
Summary
Glucocorticoids increase kidney proximal tubule cell activity by boosting NHE-3 gene transcription. This enhances the Na+/H+ antiporter
Area of Science:
- Cell Biology
- Molecular Biology
- Physiology
Background:
- OKP cells express NHE-3, an amiloride-resistant Na+/H+ antiporter crucial for proximal tubule proton secretion.
- Previous studies indicated dexamethasone, a synthetic glucocorticoid, regulates this antiporter in OKP cells.
Purpose of the Study:
- To elucidate the mechanism behind glucocorticoid-mediated increases in Na+/H+ antiporter activity.
- To investigate how dexamethasone influences NHE-3 expression and function.
Main Methods:
- OKP cells were incubated with dexamethasone (10(-6) M).
- NHE-3 mRNA abundance was quantified.
- mRNA half-life was determined.
- In vitro transcription assays were performed.
Main Results:
- Dexamethasone treatment led to a 2-3 fold increase in NHE-3 mRNA abundance within 4 hours.
- NHE-3 mRNA half-life remained stable at 8 hours in both control and treated cells.
- In vitro transcription rates increased 1.8-fold in dexamethasone-treated cells.
Conclusions:
- Glucocorticoid-induced enhancement of Na+/H+ antiporter activity is primarily mediated by an increase in NHE-3 gene transcription.
- This suggests transcriptional regulation is a key mechanism for controlling proximal tubule proton transport.