Evidence map›Paper›PMID 27336721›Full record

ArticleCell death & disease2016

Cardiac progenitor cell-derived exosomes prevent cardiomyocytes apoptosis through exosomal miR-21 by targeting PDCD4.

J Xiao, Y Pan, X H Li, X Y Yang, Y L Feng, H H Tan, L Jiang, J Feng, X Y Yu

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

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed, 3 pooled it
20.0field-weighted citation impact, top 1% 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

229 citing papers in PubMed, 3 syntheses or guidelines pooled it, 363 citations in OpenAlex.

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  20. Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025
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169 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

J XiaoSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China.
Y PanGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
X H LiGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
X Y YangSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China.
Y L FengGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
H H TanGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
L JiangGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
J FengGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
X Y YuGuangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Guangdong Academy of Medical Sciences · CNGuangdong General Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac progenitor cells derived from adult heart have emerged as one of the most promising stem cell types for cardiac protection and repair. Exosomes are known to mediate cell-cell communication by transporting cell-derived proteins and nucleic acids, including various microRNAs (miRNAs). Here we investigated the cardiac progenitor cell (CPC)-derived exosomal miRNAs on protecting myocardium under oxidative stress. Sca1(+)CPCs-derived exosomes were purified from conditional medium, and identified by nanoparticle trafficking analysis (NTA), transmission electron microscopy and western blotting using CD63, CD9 and Alix as markers. Exosomes production was measured by NTA, the result showed that oxidative stress-induced CPCs secrete more exosomes compared with normal condition. Although six apoptosis-related miRNAs could be detected in two different treatment-derived exosomes, only miR-21 was significantly upregulated in oxidative stress-induced exosomes compared with normal exosomes. The same oxidative stress could cause low miR-21 and high cleaved caspase-3 expression in H9C2 cardiac cells. But the cleaved caspase-3 was significantly decreased when miR-21 was overexpressed by transfecting miR-21 mimic. Furthermore, miR-21 mimic or inhibitor transfection and luciferase activity assay confirmed that programmed cell death 4 (PDCD4) was a target gene of miR-21, and miR-21/PDCD4 axis has an important role in anti-apoptotic effect of H9C2 cell. Western blotting and Annexin V/PI results demonstrated that exosomes pre-treated H9C2 exhibited increased miR-21 whereas decreased PDCD4, and had more resistant potential to the apoptosis induced by the oxidative stress, compared with non-treated cells. These findings revealed that CPC-derived exosomal miR-21 had an inhibiting role in the apoptosis pathway through downregulating PDCD4. Restored miR-21/PDCD4 pathway using CPC-derived exosomes could protect myocardial cells against oxidative stress-related apoptosis. Therefore, exosomes could be used as a new therapeutic vehicle for ischemic cardiac disease.

Indexed as

ApoptosisAnimalsApoptosis Regulatory ProteinsCell ShapeCytoprotectionExosomesHEK293 CellsHumansHydrogen PeroxideMaleMice, Inbred C57BLMicroRNAsModels, BiologicalMyocardiumMyocytes, CardiacOxidative StressApoptosis Regulatory ProteinsHydrogen PeroxideMicroRNAsmirn21 microRNA, ratPdcd4 protein, rat

Identifiers

PMID27336721
PMCPMC5143405
OpenAlexW2463234131

What OpenQuestion holds

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LicenceCC BY
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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.