Evidence map›Paper›PMID 31625671›Full record

ArticleJournal of cellular and molecular medicine2019

Down-regulation of GAS5 ameliorates myocardial ischaemia/reperfusion injury via the miR-335/ROCK1/AKT/GSK-3β axis.

Nan Wu, Xiaowen Zhang, Yandong Bao, Hang Yu, Dalin Jia, Chunyan Ma

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.4field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 2 institutions in 1 country.

Nan WuThe Central Laboratory of the First Affiliated Hospital of China Medical University, Shenyang, China.ORCID 0000-0002-9063-4028
Xiaowen ZhangMedical Research Center, Shengjing Hospital of China Medical University, Shenyang, China.
Yandong BaoDepartment of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Hang YuDepartment of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Dalin JiaDepartment of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Chunyan MaDepartment of Cardiovascular Ultrasound, The First Affiliated Hospital of China Medical University, Shenyang, China.
First Hospital of China Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth arrest-specific transcript 5 (GAS5), along non-coding RNA (LncRNA), is highly expressed in hypoxia/reoxygenation (H/R)-cardiomyocytes and promotes H/R-induced apoptosis. In this study, we determined whether down-regulation of GAS5 ameliorates myocardial ischaemia/reperfusion (I/R) injury and further explored its mechanism. GAS5 expression in cardiomyocytes and rats was knockdown by transfected or injected with GAS5-specific small interfering RNA or adeno-associated virus delivering small hairpin RNAs, respectively. The effects of GAS5 knockdown on myocardial I/R injury were detected by CCK-8, myocardial enzyme test, flow cytometry, TTC and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining. qRT-PCR and luciferase reporter assay were carried out to analyse the relationship between GAS5 and miR-335. The regulation of GAS5 on Rho-associated protein kinase 1 (ROCK1) expression, the activation of PI3K/AKT/GSK-3β pathway and mitochondrial permeability transition pore (mPTP) opening was further evaluated. The results indicated that GAS5 knockdown enhanced the viability, decreased apoptosis and reduced the levels of lactate dehydrogenase and creatine kinase-MB in H/R-treatment cardiomyocytes. Meanwhile, down-regulation of GAS5 limited myocardial infarct size and reduced apoptosis in I/R-heart. GAS5 was found to bind to miR-335 and displayed a reciprocal inhibition between them. Furthermore, GAS5 knockdown repressed ROCK1 expression, activated PI3K/AKT, thereby leading to inhibition of GSK-3β and mPTP opening. These suppressions were abrogated by miR-335 inhibitor treatment. Taken together, our results demonstrated that down-regulation of GAS5 ameliorates myocardial I/R injury via the miR-335/ROCK1/AKT/GSK-3β axis. Our findings suggested that GAS5 may be a new therapeutic target for the prevention of myocardial I/R injury.

Indexed as

AnimalsApoptosisCell LineCells, CulturedDown-RegulationGlycogen Synthase Kinase 3 betaMicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRats, Wistarrho-Associated KinasesRNA InterferenceRNA, Long NoncodingRNA, Small NucleolarGlycogen Synthase Kinase 3 betagrowth arrest specific transcript 5MicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktrho-Associated KinasesRNA, Long NoncodingRNA, Small NucleolarROCK1 protein, ratTransferasesgrowth arrest-specific transcript 5miR-335mitochondrial permeability transition poremyocardial ischaemia/reperfusion injuryRho-associated protein kinase 1

Identifiers

PMID31625671
PMCPMC6850918
OpenAlexW2980886661

What OpenQuestion holds

Textmetadata
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.