Evidence map›Paper›PMID 35857794›Full record

ArticlePloS one2022

ATF4 promotes brain vascular smooth muscle cells proliferation, invasion and migration by targeting miR-552-SKI axis.

Meina Feng, Qin Zhou, Wenxian Tu, Yunfeng Wang, Yuanmin Du, Kang Xu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. The Emerging Role of METTL3 in Lung Diseases.International journal of molecular sciences · 2025
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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

6 authors at 1 institution in 1 country.

Meina FengDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.ORCID 0000-0001-6950-7991
Qin ZhouDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.
Wenxian TuDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.
Yunfeng WangDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.
Yuanmin DuDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.
Kang XuDepartment of Neurology, Wuhan Brain Hospital, General Hospital of the YANGTZE River Shipping, Wuhan, China.
Yangtze Optical Electronic (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies have indicated vascular smooth muscle cells (VSMCs) played a crucial role in atherosclerosis and microRNAs (miRNAs) played key roles in biological functions of VSMCs. Whereas, the potential function and mechanism of miR-552 in VSMCs remains unclear. Our aim was to explore the role of miR-552 on VSMCs and underlying mechanism. MATERIAL/

methodsMTT assay and transwell assay were used to measure the proliferation, invasion, and migration of human brain VSMCs (HBVSMCs) and mice VSMCs (mVSMCs), respectively. Bioinformatics tools and luciferase assay were adopted to verify the association between miR-552 and SKI. Rescue experiments were employed to assess the interaction of miR-552 and SKI in modulating biological functions in HBVSMCs and mVSMCs. The expression level of transcription factors (TFs)was measured via qRT-PCR assay. The effect of ATF4 on miR-552 and SKI expression was tested by qRT-PCR or western blot assay. Finally, chromatin immunoprecipitation (ChIP) assay and JASPAR databases were used to analyze the regulatory linkage between ATF4 and miR-552.

resultsWe found that miR-552 was upregulated in HBVSMCs treated with PDGF-bb and miR-552 overexpression could promote proliferation, invasion, and migration of HBVSMCs and mVSMCs, whereas, miR-552 knockdown had the opposite impact. In addition, we also found that SKI was a direct target of miR-552, which reversed miR-552-mediated proliferation, invasion, and migration in HBVSMCs and mVSMCs. Furthermore, we also discovered that miR-552 overexpression promoted the effects of ATF4 elevation on proliferation, migration and invasion of HBVSMCs and mVSMCs, but, miR-552 decline had the opposite impact.

conclusionsATF4-miR-552-SKI axis played critical roles in the proliferation and migration of HBVSMCs and mVSMCs, which were closely involved in atherosclerosis (AS). Therefore, our findings might offer a novel therapeutic target for AS.

Indexed as

AtherosclerosisMicroRNAsActivating Transcription Factor 4AnimalsBrainCell MovementCell ProliferationCells, CulturedHumansMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleActivating Transcription Factor 4ATF4 protein, humanAtf4 protein, mouseMicroRNAsMIRN552 microRNA, human

Identifiers

PMID35857794
PMCPMC9299314
OpenAlexW4286008062

What OpenQuestion holds

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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.