Evidence map›Paper›PMID 31618402›Full record

ArticleActa cirurgica brasileira2019

Effect of miR-134 against myocardial hypoxia/reoxygenation injury by directly targeting NOS3 and regulating PI3K/Akt pathway.

Jian-Min Xiao, Ji-Jia Wang, Li-Li Sun

Open access · goldAbstract read
In one paragraph

Article in Acta cirurgica brasileira, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Frontiers in molecular neuroscience · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Advances in the Protective Mechanism of NO, HFrontiers in cardiovascular medicine · 2020
    Review
  9. CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    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

3 authors at 1 institution in 1 country.

Jian-Min XiaoMaster, Department of Cardiovascular Medicine , Daqing Oilfield General Hospital , Daqing , Heilongjiang , P.R. China . Technical procedures, interpretation of data, statistical analysis, manuscript preparation.ORCID http://orcid.org/0000-0002-9725-3367
Ji-Jia WangMaster, Department of Cardiovascular Medicine , Daqing Oilfield General Hospital , Daqing , Heilongjiang , P.R. China . Technical procedures, interpretation of data, statistical analysis, manuscript preparation.ORCID http://orcid.org/0000-0001-5371-4072
Li-Li SunMaster, Department of Geriatric Medicine , Daqing Oilfield General Hospital , Daqing , Heilongjiang , P.R. China . Conception and design of the study, critical revision.ORCID http://orcid.org/0000-0003-4695-1998
Daqing Oilfield General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo reveal the function of miR-134 in myocardial ischemia.

methodsReal-time PCR and western blotting were performed to measure the expression of miR-134, nitric oxide synthase 3 (NOS3) and apoptotic-associated proteins. Lactic dehydrogenase (LDH) assay, cell counting kit-8 (CCK-8), Hoechst 33342/PI double staining and flow cytometry assay were implemented in H9c2 cells, respectively. MiR-134 mimic/inhibitor was used to regulate miR-134 expression. Bioinformatic analysis and luciferase reporter assay were utilized to identify the interrelation between miR-134 and NOS3. Rescue experiments exhibited the role of NOS3. The involvement of PI3K/AKT was assessed by western blot analysis.

resultsMiR-134 was high regulated in the myocardial ischemia model, and miR-134 mimic/inhibitor transfection accelerated/impaired the speed of cell apoptosis and attenuated/exerted the cell proliferative prosperity induced by H/R regulating active status of PI3K/AKT signaling. LDH activity was also changed due to the different treatments. Moreover, miR-134 could target NOS3 directly and simultaneously attenuated the expression of NOS3. Co-transfection miR-134 inhibitor and pcDNA3.1-NOS3 highlighted the inhibitory effects of miR-134 on myocardial H/R injury.

conclusionThis present work puts insights into the crucial effects of the miR-134/NOS3 axis in myocardial H/R injury, delivering a potential therapeutic technology in future.

Indexed as

AnimalsApoptosisCell ProliferationHypoxiaMicroRNAsMyocardial Reperfusion InjuryNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal TransductionMicroRNAsMIRN134 microRNA, ratNitric Oxide Synthase Type IIINos3 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31618402
PMCPMC6799975
OpenAlexW2980192707

What OpenQuestion holds

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LicenceCC BY
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.