التفاصيل البيبلوغرافية
| العنوان: |
MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1. |
| المؤلفون: |
Haoyuan Deng1, Xia Chu1, Zhenfeng Song1, Xinrui Deng1, Huan Xu1, Yaxin Ye1, Songtao Li1, Qiao Zhang1, Changhao Su1,2, Ying Li1,2 liying_helen@163.com |
| المصدر: |
Cellular Physiology & Biochemistry (Karger AG). Jun2017, Vol. 42 Issue 1, p2171-2182. 12p. |
| مصطلحات موضوعية: |
*MICRORNA, *APOPTOSIS, *EPITHELIAL cells, *ATHEROSCLEROSIS, *BIOINFORMATICS, *LUCIFERASES |
| مستخلص: |
Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world. Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis. MicroRNAs (miRNAs) have been proven to be involved in the pathogenesis of atherosclerosis. However, studies of the functional role of apoptosis-related miRNAs in the endothelium during atherogenesis are limited. Methods: Cell injury and apoptosis were measured in five types of cells transfected with miR-1185 or cotransfected with miR-1185 and its inhibitor. Bioinformatics analysis and a luciferase reporter assay were used to confirm the targets of miR-1185. The effects of the targets of miR-1185 on endothelial apoptosis were determined using small-interfering RNA. Results: In this study, we first report that miR-1185 significantly promoted apoptosis in endothelial cells but not in vascular smooth muscle cells and macrophages. A mechanistic analysis showed that ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1), targets of miR-1185, mediated miR-1185-induced endothelial cell apoptosis. Conclusion: The results revealed the impact of miR-1185 on endothelial apoptosis, suggesting that miR-1185 may be a potential target for the prevention and treatment of atherosclerosis. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
