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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 1625130, 10 pages
Research Article

Impact of Atherosclerosis- and Diabetes-Related Dicarbonyls on Vascular Endothelial Permeability: A Comparative Assessment

1Russian Cardiology Research and Production Complex, Ministry of Healthcare of Russian Federation, 3rd Cherepkovskaya St. 15a, Moscow 121552, Russia
2Faculty of Fundamental Medicine, Lomonosov Moscow State University, Lomonosovsky Ave., 27, Moscow 119192, Russia

Correspondence should be addressed to Vladimir P. Shirinsky; moc.liamg@yksnirihs

Received 1 March 2017; Revised 31 May 2017; Accepted 10 September 2017; Published 2 October 2017

Academic Editor: Silvana Hrelia

Copyright © 2017 Mikhail V. Samsonov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Malondialdehyde (MDA), glyoxal (GO), and methylglyoxal (MGO) levels increase in atherosclerosis and diabetes patients. Recent reports demonstrate that GO and MGO cause vascular endothelial barrier dysfunction whereas no evidence is available for MDA. Methods. To compare the effects of MDA, GO, or MGO on endothelial permeability, we used human EA.hy926 endothelial cells as a standard model. To study cortical cytoplasm motility and cytoskeletal organization in endothelial cells, we utilized time-lapse microscopy and fluorescent microscopy. To compare dicarbonyl-modified protein band profiles in these cells, we applied Western blotting with antibodies against MDA- or MGO-labelled proteins. Results. MDA (150250 μM) irreversibly suppressed the endothelial cell barrier, reduced lamellipodial activity, and prevented intercellular contact formation. The motile deficiency of MDA-challenged cells was accompanied by alterations in microtubule and microfilament organization. These detrimental effects were not observed after GO or MGO (250 μM) administration regardless of confirmed modification of cellular proteins by MGO. Conclusions. Our comparative study demonstrates that MDA is more damaging to the endothelial barrier than GO or MGO. Considering that MDA endogenous levels exceed those of GO or MGO and tend to increase further during lipoperoxidation, it appears important to reduce oxidative stress and, in particular, MDA levels in order to prevent sustained vascular hyperpermeability in atherosclerosis and diabetes patients.