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Updated: Aug 18, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Endothelin-1 increases serum-glucocorticoid-regulated kinase-1 expression in smooth muscle cells
Sabine C Wolf1, Michael Schultze, Gabriele Sauter
1Medical Clinic III, Department of Cardiology, Hypertension and Renal Failure, University of Tuebingen, Germany. sabine.wolf@onlinehome.de
Abstract:
The mechanism of salt-sensitive hypertension is not fully understood. Several studies point to a possible role of endothelin (ET)-1 in this form of hypertension. Serum-regulated and glucocorticoid-regulated kinase-1 (SGK1) mediates trafficking of the renal epithelial sodium channel. The aim of the study was to find out whether ET-1 regulates SGK1. Rat smooth muscle cells were incubated with ET-1 (10(-7) M, 0-120 minutes). After 30 minutes a significant increase in SGK1 mRNA was found (122 +/- 4.2%), and a maximum was reached after 120 minutes (217 +/- 7.6%). Incubation of smooth muscle cells with ET-1 (10(-7) mol/L) in the presence of an ETA receptor antagonist inhibited SGK1 gene transcription (93 +/- 3.7%). Western blot analysis showed a time-dependent increase in SGK1 protein in smooth muscle cells. These data indicate that ET-1 increases SKG1 mRNA and protein concentration. Inhibition of ET-1 by ET antagonism prevented a SGK1 increase. Therefore, ET antagonism might influence blood pressure by regulating the sodium balance through reducing SGK1 gene expression.
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