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Cardiovascular disease basic research
Endothelial enriched microRNAs regulate angiotensin II-induced endothelial inflammation and migration
  1. Zhu Ni1,
  2. Yuan Wenjun2,
  3. Chen Sifeng3,
  4. Qin Yongwen1
  1. 1Department Of Cardiology, Changhai Hospital 168, Changhai Road, Shanghai, China
  2. 2Department Of Physiology And Key Lab Of Ministry Of Education In Fertility Preservation And Maintenance, Ningxia Medical University 1160, Shengli Road, Yinchuan, China
  3. 3Department Of Physiology And Pathophysiology, Fudan University, Shanghai Medical College, Shanghai, China


The initial stage of atherosclerosis is characterised by recruitment of leukocytes to activate endothelial cells (ECs). MicroRNAs (miRNAs) are a class of 19 to 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 up-regulated in angiotensin II-stimulated HUVECs, and this effect was partially reversed by over-expression of miR-155 and miR-221/222. In addition, cell adhesion assay revealed over-expression of miR-155 and miR-221/222 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-221/222 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.

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