Evidence map›Paper›PMID 29104843›Full record

ArticleCell & developmental biology2017

Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth.

Qingqing Gu, Guannan Zhao, Yinan Wang, Biao Xu, Junming Yue

Open access · bronzeAbstract read
In one paragraph

Article in Cell & developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Observational
  4. MiRNAs, lncRNAs, and circular RNAs as mediators in hypertension-related vascular smooth muscle cell dysfunction.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Review
  5. Article
  6. 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

5 authors at 2 institutions in 2 countries.

Qingqing GuDepartment of Cardiology, the Affiliated Hospital of Nantong University, Nantong, Jiangsu.
Guannan ZhaoDepartment of Pathology, the University of Tennessee Health Science Center, TN, Memphis, USA.
Yinan WangDepartment of Pathology, the University of Tennessee Health Science Center, TN, Memphis, USA.
Biao XuDepartment of Cardiology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, 210008, P. R. China.
Junming YueDepartment of Pathology, the University of Tennessee Health Science Center, TN, Memphis, USA.
University of Tennessee Health Science Center · USNanjing Drum Tower Hospital · CN

Funding

Transgenic rat overexpressing miR-21 in vascular smooth muscle cells:functional iR21HL095957 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YUE, JUNMING · 2010 to 2011
$421k
Transgenic rat overexpressing miR-15/16 cluster:functional implications in develoR03HD061420 · NICHD · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YUE, JUNMING · 2009 to 2010
$148k
NHLBI NIH HHS R21 HL095957NICHD NIH HHS R03 HD061420
6 · The paper itself

Abstract

miRNAs are a class of non-coding endogenous small RNAs that control gene expression at the posttranscriptional level and involved in cell proliferation, migration and differentiation. Dysregulation of miRNA expression is involved in a variety of human diseases including cardiovascular diseases. miRNAs have been shown to regulate vascular smooth muscle cell (VSMC) function and play vital roles in hypertension, restenosis and atherosclerosis. Here we reported that miR-16 as one of miRNAs in the miR-15 family was highly expressed in vascular smooth muscle cells (VSMCs) and involved in angiotensin II (Ang II) mediated VSMC signaling pathways. Ang II downregulated miR-16 expression in VSMCs. Lentiviral vector mediated miR-16 knockdown promoted Ang II-induced cell proliferation and migration. Moreover, silencing miR-16 enhanced Ang II induced cell cycle associated gene expression and promoted Ang II-activated cell proliferative pathways ERK1/2 and p38. Our finding demonstrated for the first time that miR-16 was a potential therapeutic target by participating in the Ang II-associated multiple signaling pathways in cardiovascular diseases.

Indexed as

Cell growthmiRNAVascular smooth muscle

Identifiers

PMID29104843
PMCPMC5665587
OpenAlexW2605568751

What OpenQuestion holds

Textmetadata
LicenceTDM
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.