Visit our Expo - Redox and Inflammation signaling 2012

Session XI: Cell death and cardiovascular diseases Poster XI, 11
Gene expression profiling in peripheral blood leukocytes from patients with arterial
hypertension
Angelica V.Timofeeva, Lyudmila E. Goryunova, George L. Khaspekov, Dmitrii A.
Kovalevskii, Andrey V. Skamrov, Olga S. Bulkina and Robert Sh. Beabealashvilli.
Russian Cardiology Reseach and Development Complex, 3rd Cherepkovskaya str. 15a,
121552, Moscow, Russia. E-mail: Angelica_T@cardio.ru
The pathogenesis of hypertension is a multifactorial process that involves the interaction of
genetic and environmental factors. In varying degrees, abnormalities of volume regulation,
enhanced vasoconstriction, and remodeling of the arterial wall contribute to the development
of hypertension. A wide variety of interdependent physiologic systems have been found to
influence blood pressure. Among these systems are baroreceptors, natriuretic peptides, the
renin-angiotensin-aldosterone system, the kinin-kallikrein system, the adrenergic receptor
system, and factors produced by blood vessels that cause vasodilation or contraction. As these
physiologic systems interact in complex fashion, it is difficult to establish the primary
abnormalities underlying blood pressure elevation for each studied patient. Since blood can be
considered as a connecting-link between all these systems, we hypothesized that circulating
blood cells may carry disease-specific information because of alterations in their local
environment. In this regard, we employed cDNA microarray technology to reveal differences
in gene expression in peripheral blood leukocytes from patients with arterial hypertension
(AH) comparing with normal individuals. Microarray results were confirmed by semiquantitative
RT-PCR. We have identified a gene expression pattern that accurately
distinguished AH patients from normal volunteers and was the same among AH patients
independently of the AH stage and the presence or absence of pharmacotherapy. We could
identify 13 AH-specific genes significantly activated compared with control group and 3
genes expressed at reduced level in AH. These genes are reffered to the cystein protease,
tyrosine phosphatase, thiol-disulfide oxidoreductase and chemokine receptor families,
transcription factors and heat shock proteins. Unfortunately, we cannot conclude from our
findings whether the changes in peripheral leukocytes gene expression are cause or
consequence of the pressure elevation in the AH, but we can speculate about the possible
implications of selected group of genes in vascular pathophysiology occurring in AH.
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