Evidence map›Paper›PMID 34055778›Full record

ArticleFrontiers in cell and developmental biology2021

EPC-Derived Exosomal miR-1246 and miR-1290 Regulate Phenotypic Changes of Fibroblasts to Endothelial Cells to Exert Protective Effects on Myocardial Infarction by Targeting ELF5 and SP1.

Yulang Huang, Lifang Chen, Zongming Feng, Weixin Chen, Shaodi Yan, Rongfeng Yang, Jian Xiao, Jiajia Gao, Debao Zhang, Xiao Ke

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-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

42 citing papers in PubMed, 57 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

10 authors at 3 institutions in 1 country.

Yulang HuangDepartmeng of Cardiology, Shenzhen Nanshan District Shekou People's Hospital, Shenzhen, China.
Lifang ChenDepartmeng of Cardiology, Shenzhen Nanshan District Shekou People's Hospital, Shenzhen, China.
Zongming FengDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Weixin ChenDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Shaodi YanDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Rongfeng YangDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Jian XiaoDepartmeng of Cardiology, Shenzhen Nanshan District Shekou People's Hospital, Shenzhen, China.
Jiajia GaoDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Debao ZhangDepartmeng of Cardiology, Shenzhen Nanshan District Shekou People's Hospital, Shenzhen, China.
Xiao KeDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNShenzhen Sixth People's Hospital · CNShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Endothelial progenitor cell (EPC)-derived exosomes have been found to be effective in alleviating MI, while the detailed mechanisms remain unclear. The present study aimed to determine the protective effects of EPC-derived exosomal miR-1246 and miR-1290 on MI-induced injury and to explore the underlying molecular mechanisms. The exosomes were extracted from EPCs; gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot and immunofluorescence staining, respectively. The angiogenesis and proliferation of human cardiac fibroblasts (HCFs) were determined by tube formation assay and immunofluorescence staining of PKH67, respectively. Luciferase reporter, CHIP, and EMSA assays determined the interaction between miR-1246/1290 and the targeted genes (EFL5 and SP1). The protective effects of miR-1246/1290 on MI were evaluated in a rat model of MI. EPC-derived exosomes significantly upregulated miR-1246 and miR-1290 expression and promoted phenotypic changes of fibroblasts to endothelial cells, angiogenesis, and proliferation in HCFs. Exosomes from EPCs with miR-1246 or miR-1290 mimics transfection promoted phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs, while exosomes from EPCs with miR-1246 or miR-1290 knockdown showed opposite effects in HCFs. Mechanistically, miR-1246 and miR-1290 from EPC-derived exosomes induced upregulation of ELF5 and SP1, respectively, by targeting the promoter regions of corresponding genes. Overexpression of both ELF5 and SP1 enhanced phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs pretreated with exosomes from EPCs with miR-1246 or miR-1290 mimics transfection, while knockdown of both EFL5 and SP1 exerted the opposite effects in HCFs. Both ELF5 and SP1 can bind to the promoter of CD31, leading to the upregulation of CD31 in HCFs. Furthermore,

Indexed as

CD31ELF5EPC-derived exosomesfibroblast-endothelial transitionmiR-1246miR-1290SP1

Identifiers

PMID34055778
PMCPMC8155602
OpenAlexW3162611475

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.