Evidence map›Paper›PMID 26992033›Full record

ArticleJournal of cellular and molecular medicine2016

Phenotypic switching of vascular smooth muscle cells in the 'normal region' of aorta from atherosclerosis patients is regulated by miR-145.

Yu-Nan Zhang, Bao-Dong Xie, Lu Sun, Wei Chen, Shu-Lin Jiang, Wei Liu, Fei Bian, Hai Tian, Ren-Ke Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 109 citations in OpenAlex.

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  13. Biomaterials science · 2023
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  20. Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022
    Review
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

9 authors at 3 institutions in 2 countries.

Yu-Nan ZhangDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Bao-Dong XieDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Lu SunDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Wei ChenDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shu-Lin JiangDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Wei LiuKey Laboratories of Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Ministry of Education, Harbin, China.
Fei BianKey Laboratories of Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Ministry of Education, Harbin, China.
Hai TianDepartment of Cardiovascular Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ren-Ke LiToronto General Research Institute, University Health Network and Department of Surgery, Division of Cardiac Surgery, University of Toronto, Toronto, ON, Canada.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Switching of vascular smooth muscle cells (VSMCs) from a contractile phenotype to an adverse proliferative phenotype is a hallmark of atherosclerosis or vascular restenosis. However, the genetic modulators responsible for this switch have not been fully elucidated in humans nor have they been correlated with clinical abnormalities. This study investigated genetic mechanisms involved in phenotypic switching of VSMCs at non-defect areas of the aorta in patients with atherosclerosis. Aortic wall samples were obtained from patients with (N = 53) and without (N = 27) atherosclerosis undergoing cardiovascular surgery. Vascular smooth muscle cell cultures were generated, and expression of microRNA-145 (miR-145), its target gene Kruppel-Like Factor 5 (KLF5) and Myocardin (MYOCD, a smooth muscle-specific transcriptional coactivator) were analysed using RT-qPCR, along with expression of relevant proteins. Vascular smooth muscle cells were transduced with miR-145 inhibitor and mimic to determine the effect of miR-145 expression on VSMC proliferation. miR-145 expression decreased while KLF5 expression increased in atherosclerotic aortas. Atherosclerotic samples and VSMCs had decreased expression of contractile markers calponin and alpha smooth muscle actin (α-SMA) and MYOCD. miR-145 inhibitor-transduced VSMCs from non-atherosclerotic patients showed decreased expression of calponin and α-SMA and increased proliferation compared with non-transduced controls, and these levels were close to those of atherosclerotic patients. miR-145 mimic-transduced VSMCs from atherosclerotic patients showed increased expression of calponin and α-SMA and decreased proliferation compared with non-transduced controls, and these levels were close to those found in non-atherosclerotic patients. These data demonstrate that miR-145 modulates the phenotypic switch of VSMCs from a contractile to a proliferative state via KLF5 and MYOCD in atherosclerosis.

Indexed as

AdultAortaAtherosclerosisBiomarkersCell ProliferationFemaleGene Expression RegulationHumansMaleMicroRNAsMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleOrgan SpecificityPhenotypeBiomarkersMicroRNAsMIRN145 microRNA, humanatherosclerosismiR-145phenotypic switchproliferationVSMCs

Identifiers

PMID26992033
PMCPMC4882986
OpenAlexW2296829780

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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.