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Myeloperoxidase oxidized LDL interferes with endothelial cell motility through miR-22 and heme oxygenase 1 induction: possible involvement in reendothelialization of vascular injuries.

Myeloperoxidase oxidized LDL interferes with endothelial cell motility through miR-22 and heme oxygenase 1 induction: possible involvement in reendothelialization of vascular injuries.

Authors :
Daher, Jalil
Martin, Maud
Rousseau, Alexandre
Nuyens, Vincent
Fayyad Kazan, Hussein
Van Antwerpen, Pierre
Courbebaisse, Guy
Martiat, Philippe
Badran, Bassam
Dequiedt, Franck
Zouaoui Boudjeltia, Karim
Vanhamme, Luc
Daher, Jalil
Martin, Maud
Rousseau, Alexandre
Nuyens, Vincent
Fayyad Kazan, Hussein
Van Antwerpen, Pierre
Courbebaisse, Guy
Martiat, Philippe
Badran, Bassam
Dequiedt, Franck
Zouaoui Boudjeltia, Karim
Vanhamme, Luc
Source :
Mediators of inflammation, 2014
Publication Year :
2014

Abstract

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.<br />SCOPUS: ar.j<br />info:eu-repo/semantics/published

Details

Database :
OAIster
Journal :
Mediators of inflammation, 2014
Notes :
1 full-text file(s): application/pdf, English
Publication Type :
Electronic Resource
Accession number :
edsoai.ocn908479355
Document Type :
Electronic Resource