Evidence map›Paper›PMID 30907506›Full record

ArticleJournal of cellular and molecular medicine2019

MicroRNA-92a promotes vascular smooth muscle cell proliferation and migration through the ROCK/MLCK signalling pathway.

Jingyu Wang, Chenxu Zhang, Cai Li, Dandan Zhao, Shuyao Li, Le Ma, Ying Cui, Xiaoqing Wei, Ying Zhao, Ying Gao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Therapeutic Potential of Modulating Gene-MicroRNA Crosstalk in Burn Injury.International journal of molecular sciences · 2025
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  7. Emerging role of exosomes in vascular diseases.Frontiers in cardiovascular medicine · 2023
    Review
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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 1 institution in 1 country.

Jingyu WangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.ORCID 0000-0002-6324-5609
Chenxu ZhangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Cai LiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Dandan ZhaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Shuyao LiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Le MaCollege of Stomatology, Dalian Medical University, Dalian, China.
Ying CuiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Xiaoqing WeiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Ying ZhaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Ying GaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To identify the interaction between known regulators of atherosclerosis, microRNA-92a (miR-92a), Rho-associated coiled-coil-forming kinase (ROCK) and myosin light chain kinase (MLCK), we examined their expressions during proliferation and migration of platelet-derived growth factor-BB (PDGF-BB)-regulated vascular smooth muscle cells (VSMCs), both in vivo and in vitro. During the formation of atherosclerosis plaque in mice, a parallel increase in expression levels of MLCK and miR-92a was observed while miR-92a expression was reduced in ML-7 (an inhibitor of MLCK) treated mice and in MLCK-deficient VSMCs. In vitro results indicated that both MLCK and miR-92a shared the same signalling pathway. Transfection of miR-92a mimic partially restored the effect of MLCK's deficiency and antagonized the effect of Y27632 (an inhibitor of ROCK) on the down-regulation of VSMCs activities. ML-7 increased the expression of Kruppel-like factor 4 (KLF4, a target of miR-92a), and siRNA-KLF4 increased VSMCs' activity level. Consistently, inhibition of either MLCK or ROCK enhanced the KLF4 expression. Moreover, we observed that ROCK/MLCK up-regulated miR-92a expression in VSMCs through signal transducer and activator of transcription 3 (STAT3) activation. In conclusion, the activation of ROCK/STAT3 and/or MLCK/STAT3 may up-regulate miR-92a expression, which subsequently inhibits KLF4 expression and promotes PDGF-BB-mediated proliferation and migration of VSMCs. This new downstream node in the ROCK/MLCK signalling pathway may offer a potential intervention target for treatment of atherosclerosis.

Indexed as

AnimalsAtherosclerosisAzepinesBecaplerminCell MovementCell ProliferationEnzyme InhibitorsHumansKruppel-Like Factor 4MaleMice, Inbred C57BLMice, KnockoutMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleMyosin-Light-Chain KinaseAzepinesBecaplerminEnzyme InhibitorsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4MicroRNAsMirn92 microRNA, mouseML 7Myosin-Light-Chain KinaseNaphthalenesrho-Associated KinasesSTAT3 Transcription FactormiR-92aMLCKROCKVSMC

Identifiers

PMID30907506
PMCPMC6484312
OpenAlexW2941033063

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.