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Visit our Expo - Redox and Inflammation signaling 2012

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Session XI: Cell death <strong>and</strong> cardiovascular diseases Poster XI, 7<br />

Atrial appendages transcriptional profile in atrial fibrillation patients with structural<br />

heart diseases.<br />

Maria S. Kharlap, Angelica V.Timofeeva, Lyudmila E. Goryunova, George L.<br />

Khaspekov, Andrey V. Skamrov, Sergey L. Dzemeshkevich, Renat S. Akchurin, Sergey<br />

P.Golitsyn <strong>and</strong> Robert Sh. Beabealashvilli.<br />

Department of Clinical Electrophysiology/Laboratory of Genetic Engineering, Russian<br />

Cardiology Research <strong>and</strong> Development Complex, 3rd Cherepkovskaya str. 15a, 121552,<br />

Moscow, Russia. E-mail: kharlapmaria@yahoo.com<br />

During the last few years several investigations devoted to gene expression analysis in human<br />

atria in patients with atrial fibrillation (AF) have been performed. The subject of those studies<br />

was atrial tissue from the patients undergoing open heart surgery with sinus rhythm <strong>and</strong> with<br />

AF. Such kind of investigations were limited by the presence of structural changes associated<br />

with underlying heart disease in control atrial tissue samples.<br />

In this regard, it seemed to be reasonable to compare the atrial tissue samples from AF<br />

patients with those from subjects without structural heart diseases. For this purpose, we<br />

employed cDNA microarray technique. Tissue samples of right atrial appendages (RAA)<br />

were obtained from 12 AF patients undergoing open heart surgery with valve disease,<br />

myxoma <strong>and</strong> coronary artery disease. Control group included 11 autopsy RAA tissue samples<br />

from people with no signs of cardiovascular diseases died during the accidents. Gene<br />

expression was analyzed using Human cDNA Expression Arrays from Clontech (total 4704<br />

genes). The results were verified by reverse transcription polymerase chain reaction. 15 genes<br />

were found to be down-regulated in AF patients independently of the type of the structural<br />

heart disease <strong>and</strong> ranged from 1.2 to 28 fold (p

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