Evidence map›Paper›PMID 27411964›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.

Hongxia Liu, Guofen Li, Wenxue Zhao, Yibo Hu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Transient miR-92a Induction in Intermediate Monocytes (CD14International journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
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  14. Article
  15. Exercise Mediates Heart Protection via Non-coding RNAs.Frontiers in cell and developmental biology · 2020
    Review
  16. lncRNA HOTAIR Protects Myocardial Infarction Rat by Sponging miR-519d-3p.Journal of cardiovascular translational research · 2019
    Article
  17. Review
  18. Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

Hongxia LiuDepartment of Clinical Laboratory Medicine, The Central Hospital of Nanyang, Nanyang, Henan, China (mainland).
Guofen LiCell Morphology Inspection of Clinical Laboratory Medicine, The Central Hospital of Nanyang, Nanyang, Henan, China (mainland).
Wenxue ZhaoDepartment of Cardiology, Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Yibo HuDepartment of Cardiopulmonary Exercise Testing, The Central Hospital of Nanyang, Nanyang, Henan, China (mainland).
Nanyang Institute of Technology · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND This study was designed to investigate the effects of microRNA-92 (miR-92), Kruppel-like factor 2 (KLF2), and Kruppel-like factor 4 (KLF4) on endothelial injury after acute myocardial infarction (AMI). MATERIAL AND METHODS Blood samples were collected from 50 AMI patients for detection of cardiac troponin I (cTnI), heart-type fatty acid-binding protein (H-FABP), and von Willebrand factor (vWF). The Sprague-Dawley rat models of AMI (n=30) were established by ligating their left anterior descending coronary artery. The cardiac markers of AMI patients and rat models were analyzed with enzyme-linked immunosorbent assay and immunohistochemistry. Human umbilical vein endothelial cells were processed into 5 groups: control, negative control, miR-92a inhibitors, miR-92a inhibitors + KLF2 small interfering RNA (siRNA), and miR-92a inhibitors + KLF4 siRNA. Cell proliferation and apoptosis were detected using MTT assay and flow cytometry. RT-PCR and Western blot were conducted to analyze KLF2 and KLF4 expressions. RESULTS AMI patients exhibited significantly higher expression of both endothelial injury markers (e.g., cTnI, H-FABP, vWF) and miR-92a in blood samples, when compared with controls (P<0.05). Model rats also had similar expressional tendencies, along with lower KLF2 and KLF4 expressions (P<0.05). Further, it could be observed in cellular experiments that treatment of miR-92a mimics can further upregulate endothelial injury markers, and miR-92a and both KLF2 and KLF4 were downregulated by miR-92a mimics (all, P<0.05). Also, the luciferase activity assay confirmed the direct binding of miR-92a to 3' UTR of KLF2/4. CONCLUSIONS MiR-92a was involved in the endothelial injury process after AMI and was able to suppress KLF2 and KLF4 expression.

Indexed as

AdultAgedAged, 80 and overAnimalsEndothelial CellsFatty Acid Binding Protein 3Fatty Acid-Binding ProteinsFemaleHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMicroRNAsMiddle AgedMyocardial InfarctionFABP3 protein, humanFatty Acid Binding Protein 3Fatty Acid-Binding ProteinsKLF2 protein, humanKlf2 protein, ratKLF4 protein, humanKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN92 microRNA, humanMIRN92 microRNA, ratRNA, Small InterferingTroponin Ivon Willebrand Factor

Identifiers

PMID27411964
PMCPMC4957625
OpenAlexW2473268362

What OpenQuestion holds

Textmetadata
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.