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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.

Supplementary Material

We showed that Mox-LDL inhibits EC motility and tubulogenesis and tried to uncover the molecular mechanisms behind this action. Supplementary Table I quantifies the expression changes of 94 genes known to be involved in angiogenesis under this Mox-LDL treatment while supplementary Tables II and III summarize the changes detected in miR expression. We showed in the «results» section that two of these expression changes are important for Mox­LDL action, namely those of HO-I and miR-22. For this purpose we used miR-22 inhibitors and supplementary Figure III illustrates a control experiment that showed that it indeed reduced Significantly miR-22 levels. We also overexpressed HO-I and showed that this was sufficient to mimick the action of Mox-LDL (supplementary Figure IV). We also attempted to uncover the final targets of HO-I action, and supplementary figures I and II suggest that this act ion is not mediated by a change in the expression or localization of the adhesion plaque components.

  1. Supplementary Materials