Open Access

miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR

  • Authors:
    • Xiaofang Sui
    • Shuqian Yu
    • Lin Dou
    • Xiehui Chen
    • Xuejie Li
    • Jun Yang
    • Yanan Su
    • Shuyue Wang
    • Fengling Wang
    • Jian Li
  • View Affiliations

  • Published online on: August 10, 2018     https://doi.org/10.3892/ijmm.2018.3821
  • Pages: 2383-2392
  • Copyright: © Sui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Endothelial dysfunction is an early marker of atherosclerosis. Previous studies have indicated that microRNA (miR)‑291b‑3p regulates the metabolism of lipids and glucose in the liver via targeting adenosine monophosphate‑activated kinase α1 and transcription factor p65. The present study investigated whether miR‑291b‑3p mediated H2O2‑mediated endothelial dysfunction. The level of apoptosis of EOMA mouse endothelial cells was analyzed by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labelling staining. The mRNA levels of miR‑291b‑3p, intercellular adhesion molecule‑1 (ICAM‑1) and vascular adhesion molecule‑1 (VCAM‑1) were determined by quantitative polymerase chain reaction. The level of phosphorylated extracellular signal‑regulated kinase, and levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and Bcl‑2 protein were detected by western blot analysis. The treatment of H2O2 induced the apoptosis and increased the mRNA levels of miR‑291b‑3p, ICAM‑1 and VCAM‑1 in EOMA cells. It was also demonstrated that the overexpression of miR‑291b‑3p promoted EOMA cell apoptosis and dysfunction. In contrast, the downregulation of miR‑291b‑3p rescued the effect of H2O2 on EOMA cell dysfunction. In addition, Hu antigen R (HuR) was identified as a target gene of miR‑291b‑3p in EOMA cells. The overexpression of HuR reversed the endothelial dysfunction induced by miR‑291b‑3p mimics. The present study provides novel insight into the critical role of miR‑291b‑3p on the endothelial dysfunction induced by H2O2. miR‑291b‑3p may mediate H2O2‑induced endothelial dysfunction via targeting HuR.
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November-2018
Volume 42 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Sui X, Yu S, Dou L, Chen X, Li X, Yang J, Su Y, Wang S, Wang F, Li J, Li J, et al: miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR. Int J Mol Med 42: 2383-2392, 2018.
APA
Sui, X., Yu, S., Dou, L., Chen, X., Li, X., Yang, J. ... Li, J. (2018). miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR. International Journal of Molecular Medicine, 42, 2383-2392. https://doi.org/10.3892/ijmm.2018.3821
MLA
Sui, X., Yu, S., Dou, L., Chen, X., Li, X., Yang, J., Su, Y., Wang, S., Wang, F., Li, J."miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR". International Journal of Molecular Medicine 42.5 (2018): 2383-2392.
Chicago
Sui, X., Yu, S., Dou, L., Chen, X., Li, X., Yang, J., Su, Y., Wang, S., Wang, F., Li, J."miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR". International Journal of Molecular Medicine 42, no. 5 (2018): 2383-2392. https://doi.org/10.3892/ijmm.2018.3821