Icariin attenuates endothelial-mesenchymal transition via H19/miR-148b-3p/ELF5 in ox-LDL-stimulated HUVECs.
Mol Ther Nucleic Acids
; 23: 464-475, 2021 Mar 05.
Article
en En
| MEDLINE
| ID: mdl-33510936
ABSTRACT
Atherosclerosis is the main cause of cardio-cerebrovascular diseases. Endothelial-mesenchymal transition plays an important role in atherosclerosis. Icariin has a protective effect on atherosclerosis; however, the underlying mechanism remains unclear. In this study, we explored the molecular mechanism underlying the protective function of icariin in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells. H19, a long non-coding RNA, was identified to be downregulated in the background of the oxidized low-density lipoprotein-induced endothelial-mesenchymal transition in human umbilical vein endothelial cells. Icariin upregulated H19 expression and inhibited the transformation of endothelial cells into interstitial cells. Overexpression of H19 affected endothelial-mesenchymal transition in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas H19 knockdown reversed endothelial protective effects of icariin and reduced human umbilical vein endothelial cell migration. Knockdown of H19 significantly downregulated oxidized low-density lipoprotein-induced E74-like factor 5 and upregulated miR-148b-3p, which was reversed by icariin. Thus, icariin may play a protective role in atherosclerosis, and H19 may be a potential therapeutic target.
Texto completo:
1
Base de datos:
MEDLINE
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Mol Ther Nucleic Acids
Año:
2021
Tipo del documento:
Article
País de afiliación:
China