التفاصيل البيبلوغرافية
| العنوان: |
Endothelial enriched microRNAs regulate angiotensin II-induced endothelial inflammation and migration |
| المؤلفون: |
Zhu, Ni, Zhang, Dongze, Chen, Sifeng, Liu, Xuemei, Lin, Li, Huang, Xinmiao, Guo, Zhifu, Liu, Juan, Wang, Yanrong, Yuan, Wenjun, Qin, Yongwen |
| سنة النشر: |
2011 |
| المجموعة: |
Xiamen University Institutional Repository |
| مصطلحات موضوعية: |
KeyWords Plus: CELL-ADHESION MOLECULE-1, VASCULAR INFLAMMATION, TRANSCRIPTION FACTORS, GENE-EXPRESSION, IN-VIVO, ATHEROSCLEROSIS, ETS-1, ANGIOGENESIS, DICER, RNAS |
| الوصف: |
Inflammation is observed at all stages of atherosclerosis. The initial stage of atherosclerosis is characterized by recruitment of leukocytes to activated endothelial cells (ECs). MicroRNAs (miRNAs) are a class of 19-25 nucleotides, non-protein-coding RNAs that repress target gene expression by translational inhibition or mRNA degradation. The link between miRNA and endothelial functions is largely unknown. Northern blot showed that miR-155 and miR-221 were highly expressed in human umbilical vein endothelial cells (HUVECs) and vascular smooth muscle cells (VSMCs). Bioinformatics analysis proposed Ets-1, a key endothelial transcription factor for inflammation and tube formation, as a candidate target for miR-155 and miR-221/222 cluster. The effect was demonstrated by luciferase reporter assay and Western blot. By using Western blot, we also confirmed that angiotensin II type 1 receptor (AT1R) is a target of miR-155 in HUVECs. Quantitative PCR showed that Ets-1 and its downstream genes, including VCAM1, MCP1 and FLT1, were upregulated in angiotensin II-stimulated HUVECs, and this effect was partially reversed by overexpression of miR-155 and miR-2211222. In addition, cell adhesion assay revealed overexpression of miR-155 and miR-2211222 effectively decreased the adhesion of Jurkat T cells to Ang II-stimulated HUVECs. Besides, by targeting AT1R, miR-155 can also decrease the HUVECs migration in response to Ang II. In summary, HUVECs highly expressed miR-155 may co-target AT1R and Ets-1 while miR-2211222 targets Ets-1, which indirectly regulate the expression of several inflammatory molecules of ECs, and therefore attenuate the adhesion of Jurkat T cells to activated HUVECs and reduce HUVECs migration. These findings present possible therapeutic targets in atherosclerosis. (C) 2011 Elsevier Ireland Ltd. All rights reserved. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| تدمد: |
0021-9150 |
| العلاقة: |
Atherosclerosis; ISI:000288940000006; http://dspace.xmu.edu.cn/handle/2288/66477Test |
| الإتاحة: |
http://dspace.xmu.edu.cn/handle/2288/66477Test |
| رقم الانضمام: |
edsbas.B04FC49E |
| قاعدة البيانات: |
BASE |
