• Citer

Apoliporotein L3 interferes with endothelial tube formation via regulation of ERK1/2, FAK and Akt signaling pathway.

par Khalil, Alia ;Poelvoorde, Philippe ;Fayyad Kazan, Mohammad ;Rousseau, Alexandre ;Nuyens, Vincent;Uzureau, Sophie ;Biston, Patrick ;El-Makhour, Yolla;Badran, Bassam ;Van Antwerpen, Pierre ;Zouaoui Boudjeltia, Karim ;Vanhamme, Luc
Référence Atherosclerosis, 279, page (73-87)
Publication Publié, 2018-10

Article révisé par les pairs

• Accès en ligne
• Détails
• Contenu
• Statistiques

Résumé :

Endothelial cells are main actors in vascular homeostasis as they regulate vascular pressure and permeability as well as hemostasis and inflammation. Disturbed stimuli delivered to and by endothelial cells correlate with the so-called endothelial dysfunction and disrupt this homeostasis. As constituents of the inner layer of blood vessels, endothelial cells are also involved in angiogenesis. Apolipoprotein Ls (APOL) comprise a family of newly discovered apolipoproteins with yet poorly understood function, and are suggested to be involved in inflammatory processes and cell death mechanisms. Here we investigate the role of APOLs in endothelial cells stimulated with factors known to be involved in atherogenesis and their possible contribution to endothelial dysfunction with an emphasis on inflammation driven-angiogenesis in vitro.