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Mediators of Inflammation
Volume 2014 (2014), Article ID 134635, 14 pages
Research Article

Myeloperoxidase Oxidized LDL Interferes with Endothelial Cell Motility through miR-22 and Heme Oxygenase 1 Induction: Possible Involvement in Reendothelialization of Vascular Injuries

1Institute for Molecular Biology and Medicine (IBMM), Université Libre de Bruxelles, rue des Professeurs Jeener et Brachet 12, 6041 Gosselies, Belgium
2Laboratory of Protein Signaling and Interactions, Interdisciplinary Cluster for Applied Genoproteomics (GIGA-R), University of Liège, Avnue de l’Hopital 1 (B34), 4000 Sart-Tilman, Belgium
3Laboratory of Experimental Medicine (ULB 222 Unit), CHU de Charleroi, A. Vésale Hospital, Université Libre de Bruxelles, rue de Gozée 706, 6110 Montigny-le-Tilleul, Belgium
4Laboratory of Experimental Hematology, Institut Jules Bordet, Université Libre de Bruxelles, Boulevard de Waterloo 121, 1000 Bruxelles, Belgium
5Laboratory of Pharmaceutical Chemistry, Faculty of Pharmacy, Université Libre de Bruxelles, Boulevard du Triomphe, Campus Plaine CP 205/5, 1050 Bruxelles, Belgium
6Creatis, CNRS UMR 5220, INSERM U1044, UCB Lyon1, INSA Lyon, University of Lyon, 7 Avenue Jean Capelle, 69621 Villeurbanne, France
7Laboratory of Immunology, Department of Biochemistry, Faculty of Sciences, Lebanese University, Hadath, Beirut 21219, Lebanon

Received 27 June 2014; Accepted 9 September 2014; Published 2 November 2014

Academic Editor: Dezheng Zhao

Copyright © 2014 Jalil Daher 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.


Cardiovascular disease linked to atherosclerosis is the leading cause of death worldwide. Atherosclerosis is mainly linked to dysfunction in vascular endothelial cells and subendothelial accumulation of oxidized forms of LDL. In the present study, we investigated the role of myeloperoxidase oxidized LDL (Mox-LDL) in endothelial cell dysfunction. We studied the effect of proinflammatory Mox-LDL treatment on endothelial cell motility, a parameter essential for normal vascular processes such as angiogenesis and blood vessel repair. This is particularly important in the context of an atheroma plaque, where vascular wall integrity is affected and interference with its repair could contribute to progression of the disease. We investigated in vitro the effect of Mox-LDL on endothelial cells angiogenic properties and we also studied the signalling pathways that could be affected by analysing Mox-LDL effect on the expression of angiogenesis-related genes. We report that Mox-LDL inhibits endothelial cell motility and tubulogenesis through an increase in miR-22 and heme oxygenase 1 expression. Our in vitro data indicate that Mox-LDL interferes with parameters associated with angiogenesis. They suggest that high LDL levels in patients would impair their endothelial cell capacity to cope with a damaged endothelium contributing negatively to the progression of the atheroma plaque.