• Citer

Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells.

par Dufour, Damien ;Khalil, Alia ;Nuyens, Vincent;Rousseau, Alexandre ;Delporte, Cédric ;Noyon, Caroline ;Cortese, Melissa ;Reye, Florence ;Pireaux, Valérie ;Neve, Jean ;Vanhamme, Luc ;Robaye, Bernard ;Lelubre, Christophe ;Desmet, Jean-Marc;Raes, Martine;Zouaoui Boudjeltia, Karim ;Van Antwerpen, Pierre
Référence Atherosclerosis, 272, page (108-117)
Publication Publié, 2018-05

Article révisé par les pairs

• Accès en ligne
• Détails
• Contenu
• Statistiques

Résumé :

Oxidation of native low-density lipoproteins (LDLs-nat) plays an important role in the development of atherosclerosis. A major player in LDL-nat oxidation is myeloperoxidase (MPO), a heme enzyme present in azurophil granules of neutrophils and monocytes. MPO produces oxidized LDLs called Mox-LDLs, which cause a pro-inflammatory response in human microvascular endothelial cells (HMEC), monocyte/macrophage activation and formation of foam cells. Resolvin D1 (RvD1) is a compound derived from the metabolism of the polyunsaturated fatty acid DHA, which promotes resolution of inflammation at the ng/ml level.