Evidence map›Paper›PMID 31220137›Full record

ArticlePloS one2019

HDL protects against myocardial ischemia reperfusion injury via miR-34b and miR-337 expression which requires STAT3.

Sarah Pedretti, Marie-Claude Brulhart-Meynet, Fabrizio Montecucco, Sandrine Lecour, Richard W James, Miguel A Frias

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  15. STAT3 Regulates miR-384 Transcription During Th17 Polarization.Frontiers in cell and developmental biology · 2019
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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 3 institutions in 3 countries.

Sarah PedrettiDepartment of Medical Specialties-Endocrinology, Diabetology, Hypertension and Nutrition, University of Geneva, Geneva, Switzerland.
Marie-Claude Brulhart-MeynetDepartment of Medical Specialties-Endocrinology, Diabetology, Hypertension and Nutrition, University of Geneva, Geneva, Switzerland.
Fabrizio MontecuccoFirst Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa School of Medicine, Genoa, Italy.
Sandrine LecourHatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Richard W JamesDepartment of Medical Specialties-Endocrinology, Diabetology, Hypertension and Nutrition, University of Geneva, Geneva, Switzerland.
Miguel A FriasDepartment of Medical Specialties-Endocrinology, Diabetology, Hypertension and Nutrition, University of Geneva, Geneva, Switzerland.ORCID 0000-0001-6884-4793
University of Geneva · CHOspedale Policlinico San Martino · ITUniversity of Cape Town · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHigh density lipoprotein (HDL) protects against myocardial infarction via mechanisms that remain unclear. STAT3 (signal transducer and activator of transcription 3) plays a key role in HDL-induced cardioprotection. In the heart, microRNAs (miRNAs) are involved in ischemia reperfusion injury. We therefore investigated whether the cardioprotective effect of HDL modulates miRNAs as a downstream target of STAT3 activation.

methodsSTAT3 cardiomyocyte deficient mice (STAT3-KO) and wildtype littermates (STAT3-WT) were submitted to left coronary ligature and reperfused (IR) with or without injection of HDL. Infarct size (IS) was determined and cardiac miRNA expression was evaluated after reperfusion in sham, IR and IR+HDL hearts by microarray analysis. In vitro, neonatal rat ventricular cardiomyocytes were submitted to hypoxia with or without HDL incubation. Cell viability and miRNA expression were analysed.

resultsIn vivo, HDL reduced IS from 40.5±4.3% to 24.4±2.1% (p<0.05) in STAT3-WT mice. HDL failed to protect in STAT3-KO mice. In STAT3-WT mice, both miR-34b and miR-337 were increased in IR compared to sham and IR+HDL groups (p<0.05). These miRNAs were not modulated in STAT3-KO mice. In vitro, incubation with HDL improved cell viability against hypoxia (p<0.05). The expression of miR-34b and miR-337 was increased by hypoxia and reduced by HDL treatment (p<0.05). In cardiomyocytes transfected with miRNA mimics, HDL failed to improve cell viability against hypoxia.

conclusionsOur study, performed both in vivo and in vitro, delineates a novel cardioprotective signalling pathway activated by HDL, involving STAT3-mediated decrease of miR-34b and miR-337 expression.

Indexed as

AnimalsApoptosisCell SurvivalHumansLipoproteins, HDLMiceMicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacPhosphorylationRatsSignal TransductionSTAT3 Transcription FactorLipoproteins, HDLMicroRNAsMIRN337 microRNA, ratMIRN34a microRNA, mouseMIRN34 microRNA, ratSTAT3 Transcription Factor

Identifiers

PMID31220137
PMCPMC6586303
OpenAlexW2950364264

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.