Evidence map›Paper›PMID 29978610›Full record

ArticleYonsei medical journal2018

Extracellular Vesicles Derived from Hypoxic Human Mesenchymal Stem Cells Attenuate GSK3β Expression via miRNA-26a in an Ischemia-Reperfusion Injury Model.

Hyewon Park, Hyelim Park, Dasom Mun, Jiyoung Kang, Hyoeun Kim, Michael Kim, Shanyu Cui, Seung Hyun Lee, Boyoung Joung

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Yonsei medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 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

9 authors at 2 institutions in 2 countries.

Hyewon ParkDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-2573-4951
Hyelim ParkDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.
Dasom MunDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.
Jiyoung KangDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.
Hyoeun KimDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.
Michael KimDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, USA.
Shanyu CuiDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.
Seung Hyun LeeBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, Korea.
Boyoung JoungDivision of Cardiology, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-9036-7225
Yonsei University · KRDuke University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeBioactive molecules critical to intracellular signaling are contained in extracellular vesicles (EVs) and have cardioprotective effects in ischemia/reperfusion (IR) injured hearts. This study investigated the mechanism of the cardioprotective effects of EVs derived from hypoxia-preconditioned human mesenchymal stem cells (MSCs). MATERIALS AND

methodsEV solutions (0.4 μg/μL) derived from normoxia-preconditioned MSCs (EV(NM)) and hypoxia-preconditioned MSCs (EV(HM)) were delivered in a rat IR injury model. Successful EV delivery was confirmed by the detection of PKH26 staining in hearts from EV-treated rats.

resultsEV(HM) significantly reduced infarct size (24±2% vs. 8±1%, p<0.001), and diminished arrhythmias by recovering electrical conduction, I(Na) current, and Cx43 expression. EV(HM) also reversed reductions in Wnt1 and β-catenin levels and increases in GSK3β induced after IR injury. miRNA-26a was significantly increased in EV(HM), compared with EV(NM), in real-time PCR. Finally, in in vitro experiments, hypoxia-induced increases in GSK3β expression were significantly reduced by the overexpression of miRNA-26a.

conclusionEV(HM) reduced IR injury by suppressing GSK3β expression via miRNA-26a and increased Cx43 expression. These findings suggest that the beneficial effect of EVHM is related with Wnt signaling pathway.

Indexed as

Reperfusion InjuryAnimalsbeta CateninConnexin 43Extracellular VesiclesGlycogen Synthase Kinase 3 betaHumansHypoxiaImmunohistochemistryIschemiaMaleMesenchymal Stem CellsMicroRNAsRatsRNA, Small Interferingbeta CateninConnexin 43CTNNB1 protein, humanGJA1 protein, humanGlycogen Synthase Kinase 3 betaGSK3B protein, humanMicroRNAsMIRN26 microRNA, humanRNA, Small InterferingarrhythmiaExtracellular vesiclesGSK3βischemia reperfusionmiRNA-26a

Identifiers

PMID29978610
PMCPMC6037597
OpenAlexW2870004355

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.