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1 Unidad de Farmacologia, Universidad de La Laguna, La Laguna, Tenerife, Spain; Cellular & Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA
2 Cellular & Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA; Farmacologia y Fisiologia, Universidad de Zaragoza, Zaragoza, Spain
3 Cellular & Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: diego.alvarez{at}ull.es.
The serum and glucocorticoid-induced kinase 1 (SGK1) is thought to be an important regulator of Na+ reabsorption in the kidney. It has been proposed that SGK1 mediates aldosterone effects on transepithelial Na+ transport. Previous studies have shown that SGK1 increases Na+ transport and epithelial Na+ channel (ENaC) activity in the apical membrane of renal epithelial cells. SGK1 has also been implicated in the modulation of Na+,K+-ATPase activity, the transporter responsible for basolateral Na+ efflux, although this observation has not been confirmed yet in renal epithelial cells. We examined Na+,K+-ATPase function in an A6 renal epithelial cell line that expresses SGK1 under the control of a tetracycline-inducible promoter. The results showed that expression of a constitutively active mutant of SGK1 (SGK1TS425D) increased by 2.5-fold the transport activity of Na+,K+-ATPase. The increase in transport activity was a direct consequence of activation of the pump itself. The onset of Na+,K+-ATPase activation was observed between 6 and 24 hours after induction of SGK1 expression, a delay that is significantly longer than the one required for activation of ENaC in the same cell line (1 hour). SGK1 and aldosterone stimulated the sodium pump synergistically, indicating that the pathways mediated by these molecules operate independently. This observation was confirmed by demonstrating that aldosterone, but not SGK1TS425D, induced approximately a 2.5-fold increase in total protein and plasma membrane Na+,K+-ATPase 
1-subunit abundance. We conclude that aldosterone increases the abundance of Na+,K+-ATPase whereas SGK1 may activate existing pumps in the membrane in response to chronic or slowly acting stimuli.
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