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Proteome Analysis Suggests That Mitochondrial Dysfunction in Stressed Endothelial Cells Is Reversed by a Soy Extract and Isolated Isoflavones

Dagmar Fuchs,^† Barbara Dirscherl,^† Joyce H. Schroot,^‡ Hannelore Daniel,^† and Uwe Wenzel*^§

Department of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich, Am Forum 5, D-85350 Freising, Germany, Food Technology Centre, part of Wageningen University and Research Centre, Bornsesteeg 59, 6708 PD Wageningen, The Netherlands, Molecular Nutrition Research, Interdisciplinary Research Center, Justus-Liebig-University of Giessen, Heinrich-Buff-Ring 26-32, D-35392 Giessen, Germany

J. Proteome Res., 2007, 6 (6), pp 2132–2142

DOI: 10.1021/pr060547y

Publication Date (Web): May 16, 2007

†

Technical University of Munich.

‡

Wageningen University and Research Centre.

To whom correspondence should be addressed. Uwe Wenzel, Molecular Nutrition Research, Interdisciplinary Research Center, Justus-Liebig-University of Giessen, Heinrich-Buff-Ring 26-32, D-35392 Giessen, Germany. Phone, +49 (0) 641/99-39220; fax, +49 (0) 641/99-39229; e-mail, uwe.wenzel@ernaehrung.uni-giessen.de.

Justus-Liebig-University of Giessen.

Abstract

Apoptosis is a driving force in atherosclerosis development. A soy extract or a combination of the soy isoflavones genistein and daidzein inhibited apoptosis induced by oxidized LDL in endothelial cells. Proteome analysis revealed that the LDL-induced alterations of numerous proteins were reversed by the extract and the genistein/daidzein mixture but only three protein entities, all functionally linked to mitochondrial dysfunction, were regulated in common by both treatments.

Keywords: proteomics • atherosclerosis • ox-LDL • apoptosis • reactive oxygen species

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