Evidence map›Paper›PMID 30784343›Full record

ArticleCell cycle (Georgetown, Tex.)

miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1.

Ming Fang, Yanfei Li, Yingbiao Wu, Zhongping Ning, Xuejun Wang, Xinming Li

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  18. Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021
    Review
  19. Article
  20. 2,3,7,8-Tetrachlorodibenzo-BioMed research international · 2020
    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

6 authors at 2 institutions in 1 country.

Ming Fanga Department of Cardiology , Hainan General Hospital , Haikou , China.
Yanfei Lib Department of Cardiology , Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.
Yingbiao Wub Department of Cardiology , Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.
Zhongping Ningb Department of Cardiology , Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.
Xuejun Wangb Department of Cardiology , Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.
Xinming Lib Department of Cardiology , Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.
Shanghai University of Medicine and Health Sciences · CNHainan General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a major risk factor for cardiovascular disease. microRNAs play a key role in gene regulation in the formation and development of atherosclerotic plaques. Herein, the role and target gene of miR-185 in AS were explored. MATERIALS AND

methodsCell viability, migration and invasion were examined by cell counting kit-8 (CCK-8) and transwell assay. The relative luciferase activity was measured by luciferase reporter assay. The levels of miR-185, STIM1, vascular endothelial growth factor (VEGF) and matrix metalloprotein-9 (MMP-9) were evaluated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot.

resultsThe results revealed that ox-LDL decreased miR-185 expression, and enhanced STIM1 expression in MOVAS cells, as well promoted cell viability, migration and invasion. 3'-UTR of STIM1 contained miR-185 binding site according to the Targetscan. miR-185 silencing or STIM1 overexpression promoted the viability, migration and invasion of ox-LDL-induced MOVAS cells. miR-185 overexpression or STIM1 silencing had the opposite effect. Besides, miR-185 silencing up-regulated the levels of VEGF and MMP-9 in vitro, and increased the lesions of arterial wall tissues and STIM1 positive rate in vivo. However, STIM1 silencing reversed these effects.

conclusionsSum up, STIM1 was a potential target gene of miR-185 in AS. Knockdown of miR-185 facilitated the progression of AS through enhancing cell proliferation, migration and invasion via targeting STIM1. The research provides a novel view of miR-185/STIM1 axis function in AS development, and this targeting method may prevent and treat AS.

Indexed as

3' Untranslated RegionsAnimalsAtherosclerosisCell LineCell MovementCell SurvivalDisease ProgressionGene Expression RegulationGene SilencingLipoproteins, LDLMatrix Metalloproteinase 9MiceMice, Inbred C57BLMicroRNAsNeoplasm InvasivenessPlaque, Atherosclerotic3' Untranslated RegionsLipoproteins, LDLMatrix Metalloproteinase 9MicroRNAsoxidized low density lipoproteinStim1 protein, mouseStromal Interaction Molecule 1Vascular Endothelial Growth Factor AatherosclerosismiR-185stromal interaction molecule 1

Identifiers

PMID30784343
PMCPMC6464577
OpenAlexW2915746785

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.