Evidence map›Paper›PMID 32308692›Full record

ArticleCellular & molecular biology letters2020

The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells.

Duo Zhao, Hao Zheng, Adam Greasley, Fengjun Ling, Qinfeng Zhou, Bowen Wang, Tiffany Ni, Ishita Topiwala, Cuilin Zhu, Tina Mele and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 13 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

12 authors at 2 institutions in 2 countries.

Duo Zhao *1Department of Cardiovascular Surgery, The Second Hospital of Jilin University, Changchun, 130041 China.
Hao Zheng *2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Adam Greasley *2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Fengjun Ling2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Qinfeng Zhou2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Bowen Wang2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Tiffany Ni2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Ishita Topiwala2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.
Cuilin Zhu1Department of Cardiovascular Surgery, The Second Hospital of Jilin University, Changchun, 130041 China.
Tina Mele5Department of Surgery, Western University, Ontario, London Canada.
Kexiang Liu1Department of Cardiovascular Surgery, The Second Hospital of Jilin University, Changchun, 130041 China.
Xiufen Zheng2Department of Pathology and Laboratory Medicine, Western University, London, Ontario Canada.ORCID 0000-0001-9988-697X
Western University · CASecond Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidative stress results in cell apoptosis/death and plays a detrimental role in disease development and progression. Stressors alter the miRNA expression profile and miRNAs play a role in the cell response to stress. We previously showed that miR-711 is significantly over-expressed in extended cold ischemia reperfusion injured hearts in heart transplant. In this study, we aimed to investigate the role of miR-711 in cardiac cell damage in response to oxidative stress and how miR-711 is regulated.

methodsRat cardiac cell line H9c2 cells were cultured and exposed to oxidative conditions (Antimycin A (AA), H

resultsWe found that miR-711 was significantly up-regulated in cells treated with H

conclusionOxidative stress increases the expression of miR-711. Over-expression of miR-711 induces cell apoptosis/death. HIF-1α and NFКB regulate miR-711 in H9c2 cells during oxidative stress. miR-711 is a new target for preventing oxidative stress.

Indexed as

Angiopoietin-1AnimalsAntimycin AApoptosisCalcium Channels, L-TypeCell HypoxiaCell LineCell SurvivalCobaltFibroblast Growth FactorsGene Knockdown TechniquesHydrogen PeroxideHypoxia-Inducible Factor 1, alpha SubunitMembrane Potential, MitochondrialMicroRNAsMitochondriaAngiopoietin-1Antimycin ACacna1c protein, ratCalcium Channels, L-TypeCobaltcobaltous chloridefibroblast growth factor 14Fibroblast Growth FactorsHif1a protein, ratHydrogen PeroxideHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN711 microRNA, ratNF-kappa BRNA, Small InterferingAng-1Cacna1cFGF14HIF-1αmiR-711NFКBOxidative stress

Identifiers

PMID32308692
PMCPMC7146913
OpenAlexW3016323355

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.