Evidence map›Paper›PMID 31597449›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2019

Extracellular MicroRNA-92a Mediates Endothelial Cell-Macrophage Communication.

Ya-Ju Chang, Yi-Shuan Li, Chia-Ching Wu, Kuei-Chun Wang, Tzu-Chieh Huang, Zhen Chen, Shu Chien

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 108 citations in OpenAlex.

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  8. Extracellular vesicles in preeclampsia: drivers of vascular dysfunction and inflammation.American journal of physiology. Heart and circulatory physiology · 2025
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  17. Lipopolysaccharide (LPS) induces sclerostin secretion by extracellular vesicle via TLR4/miR-92a-3p/PTEN/NF-κB signalling pathway in murine macrophage.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Ya-Ju ChangFrom the Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (Y.-J.C., Y.-S.L., K.-C.W., S.C.).
Yi-Shuan LiFrom the Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (Y.-J.C., Y.-S.L., K.-C.W., S.C.).
Chia-Ching WuDepartment of Cell Biology and Anatomy (C.-C.W.), College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Kuei-Chun WangFrom the Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (Y.-J.C., Y.-S.L., K.-C.W., S.C.).
Tzu-Chieh HuangInstitute of Basic Medical Sciences (C.-C.W., T.-C.H.), College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Zhen ChenDepartment of Diabetes Complications and Metabolism, Beckman Research Institute, City of Hope, Duarte, CA (Z.C.).
Shu ChienFrom the Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, La Jolla (Y.-J.C., Y.-S.L., K.-C.W., S.C.).
La Jolla Bioengineering Institute · USInstitute of Basic Medical Sciences of the Chinese Academy of Medical SciencesNational Cheng Kung University · TWUniversity of California, San Diego · US

Funding

Systems Biology Analyses for Hemodynamic Regulation of Vascular HomeostasisR01HL108735 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2012 to 2024
$13.4M
Shear Regulation of MicroRNA Transportomes and Targetomes in Vascular HomeostasisR01HL106579 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2011 to 2022
$8.3M
Role of Spatiotemporal Epigenetic Dynamics in Regulating Endothelial Gene Expressions under FlowsR01HL121365 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHIEN, SHU, WANG, YINGXIAO · 2014 to 2025
$7.5M
Locus-specific Imaging of Dynamic Histone Methylations during ReprogrammingR01GM125379 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, WANG, YINGXIAO · 2017 to 2020
$2.4M
Hypoxia-Suppressed Dicer and AGO1 Promote AngiogenesisR00HL122368 · NHLBI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHEN, ZHEN BOUMAN · 2017 to 2019
$747k
Flow Regulation of YAP/TAZ in Atherogenesis and Therapeutic DevelopmentR00HL135416 · NHLBI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI WANG, MARK KUEI-CHUN · 2020 to 2022
$740k
Flow Regulation of YAP/TAZ in Atherogenesis and Therapeutic DevelopmentK99HL135416 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, MARK KUEI-CHUN · 2017 to 2018
$272k
NHLBI NIH HHS K99 HL135416NHLBI NIH HHS R00 HL122368NHLBI NIH HHS R00 HL135416NHLBI NIH HHS R01 HL106579NHLBI NIH HHS R01 HL108735NHLBI NIH HHS R01 HL121365NIGMS NIH HHS R01 GM125379
6 · The paper itself

Abstract

objectiveUnderstanding message delivery among vascular cells is essential for deciphering the intercellular communications in cardiovascular diseases. MicroRNA (miR)-92a is enriched in endothelial cells (ECs) and circulation under atheroprone conditions. Macrophages are the primary immune cells in atherosclerotic lesions that modulate lesion development. Therefore, we hypothesize that, in response to atheroprone stimuli, ECs export miR-92a to macrophages to regulate their functions and enhance atherosclerotic progression. Approach and Results: We investigated the macrophage functions that are regulated by EC miR-92a under atheroprone microenvironments. We first determined the distributions of functional extracellular miR-92a by fractionating the intravesicular and extravesicular compartments from endothelial conditioned media and mice serum. The results indicate that extracellular vesicles are the primary vehicles for EC miR-92a transportation. Overexpression of miR-92a in ECs enhanced the proinflammatory responses and low-density lipoprotein uptake, while impaired the migration, of cocultured macrophage. Opposite effects were found in macrophages cocultured with ECs with miR-92a knockdown. Further analyses demonstrated that intravesicular miR-92a suppressed the expression of target gene

conclusionsEC miR-92a can be transported to macrophages through extracellular vesicles to regulate KLF4 levels, thus leading to the atheroprone phenotypes of macrophage and, hence, atherosclerotic lesion formation.

Indexed as

AnimalsAtherosclerosisCell CommunicationCells, CulturedExtracellular FluidHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Factor 4Kruppel-Like Transcription FactorsMacrophagesMiceMicroRNAsMicroscopy, Electron, TransmissionKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN92 microRNA, humanatherosclerosisendothelial cellsextracellular vesiclesmacrophagesmicroRNA

Identifiers

PMID31597449
PMCPMC6879873
OpenAlexW2980258469

What OpenQuestion holds

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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.