Oxidized low density lipoprotein induces endothelial-to-mesenchymal transition by stabilizing Snail in human aortic endothelial cells - 25/08/18
, Yuhan Sun b, Ziliang Ye b, Huafeng Yang b, Lang Li bBienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
Highlights |
• | ox-LDL, but not LDL, induces EndMT in human aortic endothelial cells. |
• | x-LDL-induced EndMT strictly depends on the presence of its innate receptor LOX-1. |
• | ox-LDL upregulates transcriptional factor Snail, which is essential for orchestrating x-LDL-induced EndMT. |
• | ox-LDL induces Snail stabilization by inhibiting its ubiquitination, partially due to inhibited GSK-3β. |
Abstract |
The endothelial-to-mesenchymal transition (EndMT) of endothelial cells contributes to the development of atherosclerosis. Oxidized low density lipoprotein (ox-LDL) is a highly risk factor for atherosclerosis. However, whether ox-LDL causes EndMT and the underlying mechanism are unclear. We report here that ox-LDL treatment is able to induce EndMT in human aortic endothelial cells (HAECs), and that the ox-LDL-induced EndMT is strictly dependent on the presence of its innate receptor, ox-LDL Receptor-1 (LOX-1). In addition, ox-LDL specifically upregulates EndMT transcriptional factor Snail, and knockdown of Snail completely attenuates ox-LDL-induced EndMT, indicating an essential role of Snail in mediating this effect. Mechanically, ox-LDL induces Snail stabilization by inhibiting its ubiquitination, which is in part attributed to inhibited GSK-3β activity. Hence, our findings suggest that inducing EndMT of aortic endothelial cells by ox-LDL might contribute to its detrimental role in promoting atherosclerosis development.
Le texte complet de cet article est disponible en PDF.Keywords : Ox-LDL, EndMT, Snail, HAECs, Atherosclerosis
Plan
Vol 106
P. 1720-1726 - octobre 2018 Retour au numéro
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