PMID- 30015881
OWN - NLM
STAT- MEDLINE
DCOM- 20181026
LR  - 20211204
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 18
IP  - 3
DP  - 2018 Sep
TI  - MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein 
      endothelial cells by targeting the PI3K/Akt/mTOR pathway.
PG  - 2798-2806
LID - 10.3892/mmr.2018.9236 [doi]
AB  - Endothelial cell autophagy has a protective role in inhibiting in fl ammation 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‑alpha 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.
FAU - Yin, Shuangshuang
AU  - Yin S
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Yang, Shaonan
AU  - Yang S
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Pan, Xudong
AU  - Pan X
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Ma, Aijun
AU  - Ma A
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Ma, Juanjuan
AU  - Ma J
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Pei, Haotian
AU  - Pei H
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Dong, Yi
AU  - Dong Y
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Li, Shu
AU  - Li S
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Li, Wei
AU  - Li W
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
FAU - Bi, Xinran
AU  - Bi X
AD  - Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong 266003, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180629
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Antagomirs)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (MIRN155 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RHEB protein, human)
RN  - 0 (Ras Homolog Enriched in Brain Protein)
RN  - 0 (oxidized low density lipoprotein)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Antagomirs/metabolism
MH  - Autophagy/*drug effects
MH  - Base Sequence
MH  - Human Umbilical Vein Endothelial Cells
MH  - Humans
MH  - Lipoproteins, LDL/*toxicity
MH  - MicroRNAs/antagonists & inhibitors/genetics/*metabolism
MH  - Phosphatidylinositol 3-Kinase/chemistry/genetics/*metabolism
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - Ras Homolog Enriched in Brain Protein/chemistry/genetics/metabolism
MH  - Sequence Alignment
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/genetics/*metabolism
PMC - PMC6102700
EDAT- 2018/07/18 06:00
MHDA- 2018/10/27 06:00
PMCR- 2018/06/29
CRDT- 2018/07/18 06:00
PHST- 2017/10/31 00:00 [received]
PHST- 2018/06/07 00:00 [accepted]
PHST- 2018/07/18 06:00 [pubmed]
PHST- 2018/10/27 06:00 [medline]
PHST- 2018/07/18 06:00 [entrez]
PHST- 2018/06/29 00:00 [pmc-release]
AID - mmr-18-03-2798 [pii]
AID - 10.3892/mmr.2018.9236 [doi]
PST - ppublish
SO  - Mol Med Rep. 2018 Sep;18(3):2798-2806. doi: 10.3892/mmr.2018.9236. Epub 2018 Jun 
      29.