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Horm Metab Res 2012; 44(03): 234-238
DOI: 10.1055/s-0031-1291272
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Aldosterone does not Modify Gene Expression in Human Endothelial Cells

A. Verhovez
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
,
T. A. Williams
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
,
F. Morello
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
,
S. Monticone
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
,
M. F. Brizzi
2   Department of Internal Medicine, University of Torino, Torino, Italy
,
P. Dentelli
2   Department of Internal Medicine, University of Torino, Torino, Italy
,
F. Fallo
3   Department of Medical and Surgical Sciences, University of Padova, Padova, Italy
,
B. Fabris
4   Department of Medical, Technological and Translational Sciences, University of Trieste, Cattinara Hospital, Trieste, Italy
,
F. Amenta
5   Section of Human Anatomy, School of Pharmacy, University of Camerino, Camerino (MC), Italy
,
C. Gomez-Sanchez
6   Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center and University of Mississippi Medical Center, Jackson, MS, USA
,
F. Veglio
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
,
P. Mulatero
1   Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy
› Author Affiliations
Further Information

Publication History

received 15 May 2011

accepted 26 September 2011

Publication Date:
08 November 2011 (online)

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Abstract

The toxic effects of aldosterone on the vasculature, and in particular on the endothelial layer, have been proposed as having an important role in the cardiovascular pathology observed in mineralocorticoid-excess states. In order to characterize the genomic molecular mechanisms driving the aldosterone-induced endothelial dysfunction, we performed an expression microarray on transcripts obtained from both human umbilical vein endothelial cells and human coronary artery endothelial cells stimulated with 10 − 7 M aldosterone for 18 h. The results were then subjected to qRT-PCR confirmation, also including a group of genes known to be involved in the control of the endothelial function or previously described as regulated by aldosterone. The state of activation of the mineralocorticoid receptor was investigated by means of a luciferase-reporter assay using a plasmid encoding a mineralocorticoid and glucocorticoid-sensitive promoter. Aldosterone did not determine any significant change in gene expression in either cell type both in the microarray and in the qRT-PCR analysis. The luciferase-reporter assay showed no activation of the mineralocorticoid receptor following aldosterone stimulation. The status of nonfunctionality of the mineralocorticoid receptor expressed in cultured human umbilical and coronary artery endothelial cells does not allow aldosterone to modify gene expression and provides evidence against either a beneficial or harmful genomic effect of aldosterone on healthy endothelial cells.

Key words

mineralocorticoid - endothelial dysfunction - genomic
 

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