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Articles in PresS, published online ahead of print August 27, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00028.2002
Submitted on January 22, 2002
Accepted on August 20, 2002
1 Departments of Pediatrics, and Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA
* To whom correspondence should be addressed. E-mail: cuc{at}po.cwru.edu.
The effects of the Extracellular signal-Regulated protein Kinase (ERK) pathway on electrogenic transepithelial sodium absorption by renal collecting duct cells were determined. Approximately 90% of the unstimulated short-circuit current (ISC, 15 ± 1 µA/cm2; n= 10) across conditionally-immortalized murine collecting duct epithelial cells (mCT1) is amiloride-sensitive and is likely mediated by apical epithelial sodium channels (ENaC). Chronic exposure (24 hours) of the epithelial monolayers to either epidermal growth factor (EGF; 50 ng/ml) or transforming growth factor-alpha (TGF-
; 20 ng/ml) reduced amiloride-sensitive I,SC by more than 60%. The inhibitory effect of EGF on sodium absorption was not due to inhibition of basolateral Na+-K+-ATPase, since the pump current elicited by permeabilization of apical membrane with nystatin was not reduced by EGF. Chronic exposure of the mCT1 cells to EGF (20 ng/ml; 24 hours) elicited a 70-85% decrease in ENaC subunit mRNA levels. Exposure of mCT1 cells to either EGF (20 ng/ml) or PMA (150 nM) induced rapid phosphorylation of p42/p44 (ERK1/2) and pretreatment of the monolayers with PD98059 (30 µM; MEK inhibitor) prevented phosphorylation of p42/p44. Similarly, pretreatment of mCT1 monolayers with PD98059 prevented the EGF- and PMA-induced inhibition of amiloride-sensitive sodium absorption. The results of these studies demonstrate that amiloride-sensitive sodium absorption by renal collecting duct cells is regulated by the extracellular signal-regulated protein kinase pathway. This pathway may play a role in alterations in ion transport that occur in polycystic kidney disease.
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