Evidence map›Paper›PMID 30015881›Full record

ArticleMolecular medicine reports2018

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

Shuangshuang Yin, Shaonan Yang, Xudong Pan, Aijun Ma, Juanjuan Ma, Haotian Pei, Yi Dong, Shu Li, Wei Li, Xinran Bi

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Shuangshuang YinDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Shaonan YangDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Xudong PanDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Aijun MaDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Juanjuan MaDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Haotian PeiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Yi DongDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Shu LiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Wei LiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Xinran BiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

3' Untranslated RegionsAntagomirsAutophagyBase SequenceHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLMicroRNAsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRas Homolog Enriched in Brain ProteinSequence AlignmentSignal TransductionTOR Serine-Threonine Kinases3' Untranslated RegionsAntagomirsLipoproteins, LDLMicroRNAsMIRN155 microRNA, humanMTOR protein, humanoxidized low density lipoproteinPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRas Homolog Enriched in Brain ProteinRHEB protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID30015881
PMCPMC6102700
OpenAlexW2811174919

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.