Evidence map›Paper›PMID 32626987›Full record

ArticleMolecular medicine reports2020

Downregulation of microRNA‑106a‑5p alleviates ox‑LDL‑mediated endothelial cell injury by targeting STAT3.

Ying Hu, Rong Xu, Yue He, Zhibo Zhao, Xudong Mao, Ling Lin, Jun Hu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
  6. Article
  7. MiR-106a-5p by TargetingAnimals : an open access journal from MDPI · 2024
    Article
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  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Article
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

7 authors at 1 institution in 1 country.

Ying Hu *Department of Geriatrics, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Rong Xu *Department of Geriatrics, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Yue He *Department of Cardiology, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Zhibo ZhaoDepartment of Cardiology, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Xudong MaoDepartment of Geriatrics, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Ling LinDepartment of Geriatrics, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Jun HuDepartment of Geriatrics, The Central Hospital of Xuhui District, Shanghai 200031, P.R. China.
Shanghai Xuhui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The apoptosis of endothelial cells (ECs) induced by oxidized low‑density lipoprotein (ox‑LDL) is an important contributing factor in the pathogenesis of atherosclerosis. It has been reported that microRNA (miR)‑106a‑5p is overexpressed in atherosclerotic plaques and involved in angiogenesis. However, its role and underlying mechanisms in ox‑LDL induced EC apoptosis remain to be fully understood. In the present study the expression of miR‑106a‑5p in human umbilical vein ECs (HUVECs) stimulated with ox‑LDL was investigated using reverse transcription‑quantitative PCR analysis. Cell viability and apoptosis were assessed by MTT assay and flow cytometry, respectively. Caspase‑3 activity and reactive oxygen species (ROS) levels were determined by commercial kits. The interaction between miR‑106a‑5p and signal transducer and activator of transcription 3 (STAT3) mRNA was examined by luciferase reporter assay. It was found that ox‑LDL treatment significantly increased the levels of miR‑106a‑5p in a dose‑dependent manner in HUVECs. Moreover, these results demonstrated that ox‑LDL treatment inhibited cell viability, promoted cell apoptosis, increased caspase‑3 activity and ROS levels, whereas inhibition of miR‑106a‑5p reversed the effects of ox‑LDL on HUVECs. In addition, it was shown that STAT3 is a direct target of miR‑106a‑5p in HUVECs, and silencing of STAT3 impaired the protective effects of miR‑106a‑5p inhibition on cell apoptosis and oxidative injury induced by ox‑LDL. Collectively, these results indicated that miR‑106a‑5p participated in ox‑LDL‑stimulated apoptosis and oxidative injury in HUVECs by regulating STAT3. Thus, suggesting that miR‑106a‑5p/STAT3 may serve as a novel therapeutic target for atherosclerosis in the future.

Indexed as

ApoptosisAtherosclerosisCaspase 3Cells, CulturedCell SurvivalDown-RegulationGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLMicroRNAsOxidative StressReactive Oxygen SpeciesRNA, Small InterferingSTAT3 Transcription FactorCASP3 protein, humanCaspase 3Lipoproteins, LDLMicroRNAsMIRN106 microRNA, humanoxidized low density lipoproteinReactive Oxygen SpeciesRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription Factorapoptosisatherosclerosiscell viabilityendothelial cellshuman umbilical vein endothelial cellsmicrorna-106a-5poxidized low-density lipoprotein

Identifiers

PMID32626987
PMCPMC7339537
OpenAlexW3024320214

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.