Evidence map›Paper›PMID 28751690›Full record

ArticleScientific reports2017

microRNA-352 regulates collateral vessel growth induced by elevated fluid shear stress in the rat hind limb.

Yinglu Guan, Baizhen Cai, Xiaoqiong Wu, Song Peng, Liaoying Gan, Da Huang, Guangmin Liu, Liping Dong, Lin Xiao, Junwen Liu and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

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  10. MicroRNA-146a Regulates Perfusion Recovery in Response to Arterial OcclusionFrontiers in bioengineering and biotechnology · 2018
    Article
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

14 authors at 3 institutions in 2 countries.

Yinglu GuanDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Baizhen CaiDepartment of Intensive Care Unit, the 3rd Xiangya Hospital, Central South University Changsha, 410013, Hunan, P.R. China.
Xiaoqiong WuDepartment of Anatomy & Neurobiology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Song PengDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Liaoying GanDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Da HuangDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Guangmin LiuDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Liping DongDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Lin XiaoDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Junwen LiuDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China.
Bin ZhangDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China. coolzhangbin22@163.com.
Wei-Jun CaiDepartment of Histology & Embryology, School of Basic Medicine, Central South University Changsha, 410013, Hunan, P.R. China. caiweijun@csu.edu.cn.
Jutta SchaperMax-Planck-Institute for Heart and Lung Research, Arteriogenesis Research Group, Bad Nauheim, D-61231, Germany. jutta.schaper@mpi-bn.mpg.de.
Wolfgang SchaperMax-Planck-Institute for Heart and Lung Research, Arteriogenesis Research Group, Bad Nauheim, D-61231, Germany.
Central South University · CNMax Planck Institute for Heart and Lung Research · DEXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although collateral vessel growth is distinctly enhanced by elevated fluid shear stress (FSS), the underlying regulatory mechanism of this process remains incompletely understood. Recent studies have shown that microRNAs (miRNAs) play a pivotal role in vascular development, homeostasis and a variety of diseases. Therefore, this study was designed to identify miRNAs involved in elevated FSS-induced collateral vessel growth in rat hind limbs. A side-to-side arteriovenous (AV) shunt was created between the distal stump of one of the bilaterally occluded femoral arteries and the accompanying vein. The miRNA array profile showed 94 differentially expressed miRNAs in FSS-stressed collaterals including miRNA-352 which was down-regulated. Infusion of antagomir-352 increased the number and proliferation of collateral vessels and promoted collateral flow restoration in a model of rat hind limb ligation. In cell culture studies, the miR-352 inhibitor increased endothelial proliferation, migration and tube formation. In addition, antagomir-352 up-regulated the expression of insulin-like growth factor II receptor (IGF2R), which may play a part in the complex pathway leading to arterial growth. We conclude that enhanced collateral vessel growth is controlled by miRNAs, among which miR-352 is a novel candidate that negatively regulates arteriogenesis, meriting additional studies to unravel the pathways leading to improved collateral circulation.

Indexed as

Neovascularization, PhysiologicSignal TransductionStress, PhysiologicalAnimalsCell ProliferationGene Expression ProfilingGene Expression RegulationHindlimbMicroRNAsRatsReceptor, IGF Type 2Stress, MechanicalMicroRNAsMIRN352 microRNA, ratReceptor, IGF Type 2

Identifiers

PMID28751690
PMCPMC5532297
OpenAlexW2737119333

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.