Evidence mapPaperPMID 30645204Full record

ArticleThe Journal of clinical investigation2019

Platelet-derived miR-223 promotes a phenotypic switch in arterial injury repair.

Zhi Zeng, Luoxing Xia, Xuejiao Fan, Allison C Ostriker, Timur Yarovinsky, Meiling Su, Yuan Zhang, Xiangwen Peng, Yi Xie, Lei Pi and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
14.8field-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

67 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  17. Review
  18. MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024
    Review
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

Zhi ZengInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Luoxing XiaInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Xuejiao FanInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Allison C OstrikerYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Timur YarovinskyYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Meiling SuInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Yuan ZhangInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Xiangwen PengInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Yi XieYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Lei PiDepartment of Clinical Biological Resource Bank, Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Xiaoqiong GuDepartment of Clinical Biological Resource Bank, Department of Clinical Laboratory, Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Sookja Kim ChungSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Kathleen A MartinYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Renjing LiuAgnes Ginges Laboratory for Diseases of the Aorta, Centenary Institute, and.
John HwaYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Wai Ho TangInstitute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Guangzhou Medical University · CNYale University · USGuangzhou Women and Children Medical Center · CNThe University of Sydney · AUUniversity of Hong Kong · HK

Funding

Platelets in vascular injury repairR01HL150515 · NHLBI · YALE UNIVERSITY · PI JOHN HWA · 2022 to 2023
$1.1M
NHLBI NIH HHS R01 HL115247NHLBI NIH HHS R01 HL119529NHLBI NIH HHS R01 HL122815NHLBI NIH HHS R01 HL142090NHLBI NIH HHS R01 HL150515NHLBI NIH HHS U54 HL117798
6 · The paper itself

Abstract

Upon arterial injury, endothelial denudation leads to platelet activation and delivery of multiple agents (e.g., TXA2, PDGF), promoting VSMC dedifferentiation and proliferation (intimal hyperplasia) during injury repair. The process of resolution of vessel injury repair, and prevention of excessive repair (switching VSMCs back to a differentiated quiescent state), is poorly understood. We now report that internalization of APs by VSMCs promotes resolution of arterial injury by switching on VSMC quiescence. Ex vivo and in vivo studies using lineage tracing reporter mice (PF4-cre × mT/mG) demonstrated uptake of GFP-labeled platelets (mG) by mTomato red-labeled VSMCs (mT) upon arterial wire injury. Genome-wide miRNA sequencing of VSMCs cocultured with APs identified significant increases in platelet-derived miR-223. miR-223 appears to directly target PDGFRβ (in VSMCs), reversing the injury-induced dedifferentiation. Upon arterial injury, platelet miR-223-KO mice exhibited increased intimal hyperplasia, whereas miR-223 mimics reduced intimal hyperplasia. Diabetic mice with reduced expression of miR-223 exhibited enhanced VSMC dedifferentiation and proliferation and increased intimal hyperplasia. Our results suggest that horizontal transfer of platelet-derived miRNAs into VSMCs provides a novel mechanism for regulating VSMC phenotypic switching. Platelets thus play a dual role in vascular injury repair, initiating an immediate repair process and, concurrently, a delayed process to prevent excessive repair.

Indexed as

ArteriesCell DifferentiationCell ProliferationRegenerationAnimalsBlood PlateletsCell LineDiabetes Mellitus, ExperimentalFemaleHumansMaleMiceMice, KnockoutMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleMicroRNAsMIR223, humanMIRN223 microRNA, mouseCardiovascular diseaseVascular Biology

Identifiers

PMID30645204
PMCPMC6391113
OpenAlexW2911198183

What Socratic holds

Textmetadata
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 Socratic graph.