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Proteomic Analysis of Early Left Ventricular Hypertrophy Secondary to Hypertension: Modulation by Antihypertensive Therapies

Julio Gallego-Delgado^*, Alberto Lazaro^*, Julio I. Osende, Vanesa Esteban^*, Maria G. Barderas, Carmen Gomez-Guerrero^*, Ricardo Vega^*, Fernando Vivanco^, and Jesus Egido^*

^* Renal and Vascular Pathology Laboratory, Fundación Jiménez Díaz-Universidad Autónoma, Cardiology Service, Hospital Universitario "Gregorio Maranon," Department of Inmunology, Fundación Jiménez Díaz, and Department of Biochemistry and Molecular Biology I. Proteomics Unit, Complutense University, Madrid, Spain

Address correspondence to: Dr. Jesús Egido, Renal and Vascular Laboratory, Fundación Jiménez Díaz, Avda Reyes Católicos 2, 28040, Madrid, Spain. Phone: +34-91-550-4800, ext. 3362; Fax: +34-91-549-4764; E-mail: jegido{at}fjd.es

Untreated or poorly controlled arterial hypertension induced development of pathologic left ventricular hypertrophy (LVH), a common finding in hypertensive patients and a strong predictor of cardiovascular morbidity and mortality. The proteomic approach is a powerful technique to analyze a complex mixture of proteins in various settings. An experimental model of hypertension-induced early LVH was performed in spontaneously hypertensive rats, and the cardiac protein pattern compared with the normotensive Wistar Kyoto counterpart was analyzed. Fifteen altered protein spots were shown in the early stage of LVH. Compared with a previous animal model of established and regressed LVH, three protein spots were common in both models. These three altered protein spots corresponded to two unique proteins that were identified as Calsarcin-1 (CS-1) and ubiquinone biosynthesis protein COQ7 homolog. CS-1 is a negative regulator of the calcineurin/NF-AT pathway. Because upregulation in the expression levels of this protein was observed, the activation level of NF-B by oxidative stress as an alternative pathway was investigated. It was found that antihypertensive therapies partially decreased oxidative stress and normalized the activation of NF-B in the kidneys and aorta NF-B activation but just moderately in the heart. This could be due to the interaction of any specific cardiac protein with any component of the NF-B pathway. In this sense, CS-1 could be a good candidate because it is expressed preferentially in heart, to a lesser extent in smooth muscle cells, but not in kidney. Further investigations are necessary to elucidate the exact role of CS-1 and ubiquinone biosynthesis protein COQ7 in the setting of hypertension-induced LVH.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673