期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 106, 期 -, 页码 1720-1726出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.07.122
关键词
Ox-LDL; EndMT; Snail; HAECs; Atherosclerosis
资金
- National Natural Science Foundation of China [81600283]
- Guangxi Natural Science Foundation [2017GXNSFAA198069]
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-LDLinduced 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-3 beta 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.
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