Open Access

MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway

  • Authors:
    • Shuangshuang Yin
    • Shaonan Yang
    • Xudong Pan
    • Aijun Ma
    • Juanjuan Ma
    • Haotian Pei
    • Yi Dong
    • Shu Li
    • Wei Li
    • Xinran Bi
  • View Affiliations

  • Published online on: June 29, 2018     https://doi.org/10.3892/mmr.2018.9236
  • Pages: 2798-2806
  • Copyright: © Yin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Endothelial cell autophagy has a protective role in inhibiting inflammation and preventing the development of atherosclerosis, which may be regulated by microRNA (miR)‑155. The present study aimed to investigate the mechanisms of autophagy in the development of atherosclerosis. Human umbilical vein endothelial cells model in vitro and using oxidized low‑density lipoprotein (ox‑LDL) stimulated cells to simulate the atherosclerosis. MiR‑155 mimics, miR‑155 inhibitors, and a negative control were respectively transfected in human umbilical vein endothelial cells to analyzed alterations in the expression of miR‑155. It was demonstrated that overexpression of miR‑155 promoted autophagic activity in oxidized low‑density lipoprotein‑stimulated human umbilical vein endothelial cells, whereas inhibition of the expression of miR‑155 reduced autophagic activity. Overexpression of miR‑155 revealed that it regulated autophagy via the phosphatidylinositol‑3 kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (Akt)/mechanistic target of rapamycin pathway (mTOR) signaling pathway. A luciferase reporter assay demonstrated that miR‑155 directly bound to the PI3K catalytic subunit a and Ras homolog enriched in brain 3'‑untranslated region and inhibited its luciferase activity. Therefore, the results of the present study suggested that miR‑155 promoted autophagy in vascular endothelial cells and that this may have occurred via targeting of the PI3K/Akt/mTOR pathway. Thus, miR‑155 may be considered as a potential therapeutic target for the treatment of atherosclerosis.
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September-2018
Volume 18 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Yin S, Yang S, Pan X, Ma A, Ma J, Pei H, Dong Y, Li S, Li W, Bi X, Bi X, et al: MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway. Mol Med Rep 18: 2798-2806, 2018.
APA
Yin, S., Yang, S., Pan, X., Ma, A., Ma, J., Pei, H. ... Bi, X. (2018). MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway. Molecular Medicine Reports, 18, 2798-2806. https://doi.org/10.3892/mmr.2018.9236
MLA
Yin, S., Yang, S., Pan, X., Ma, A., Ma, J., Pei, H., Dong, Y., Li, S., Li, W., Bi, X."MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway". Molecular Medicine Reports 18.3 (2018): 2798-2806.
Chicago
Yin, S., Yang, S., Pan, X., Ma, A., Ma, J., Pei, H., Dong, Y., Li, S., Li, W., Bi, X."MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway". Molecular Medicine Reports 18, no. 3 (2018): 2798-2806. https://doi.org/10.3892/mmr.2018.9236