Evidence map›Paper›PMID 29664809›Full record

ArticleJournal of hypertension2018

MicroRNA-19a/b-3p protect the heart from hypertension-induced pathological cardiac hypertrophy through PDE5A.

Kun Liu, Qiongyu Hao, Jie Wei, Gong-Hao Li, Yong Wu, Yun-Feng Zhao

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of hypertension, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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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 5 institutions in 2 countries.

Kun LiuThe Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu, PR China.
Qiongyu HaoDepartment of Cell Biology, New York University School of Medicine, New York, New York, USA.
Jie WeiDepartment of Basic Medical Sciences, Medical College, Xiamen University, Xiamen.
Gong-Hao LiThe Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu, PR China.
Yong WuDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science.
Yun-Feng ZhaoThe Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu, PR China.
Xuzhou Medical College · CNCharles R. Drew University of Medicine and Science · USNew York University · USThe First People’s Hospital of Lianyungang · CNXiamen University · CN

Funding

Mechanisms behind hyperglycemia-associated breast cancer risk and progressionSC1CA200517 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2015 to 2018
$1.4M
NCI NIH HHS SC1 CA200517
6 · The paper itself

Abstract

aimPDE5A is a leading factor contributing to cGMP signaling and cardiac hypertrophy. However, microRNA-mediated posttranscriptional regulation of PDE5A has not been reported. The aim of this study is to screen the microRNAs that are able to regulate PDE5A and explore the function of the microRNAs in cardiac hypertrophy and remodeling. METHODS AND

resultsAlthough miR-19a/b-3p (microRNA-19a-3p and microRNA-19b-3p) have been reported to be differentially expressed during cardiac hypertrophy, the direct targets and the functions of this microRNA family for regulation of cardiac hypertrophy have not yet been investigated. The present study identified some direct targets and the underlying functions of miR-19a/b-3p by using bioinformatics tools and gene manipulations within mouse neonatal cardiomyocytes. Transfection of miR-19a/b-3p down-regulated endogenous expressions of PDE5A at both mRNA and protein levels with real-time PCR and western blot. Luciferase reporter assays showed that PDE5A was a direct target of miR-19a/b-3p. In mouse models of cardiac hypertrophy, we found that miR-19a/b-3p was expressed in cardiomyocytes and that its expression was reduced in pressure overload-induced hypertrophic hearts. miR-19a/b-3p transgenic mice prevented the progress of cardiac hypertrophy and cardiac remodeling in response to angiotensin II infusion with echocardiographic assessment and pressure-volume relation analysis.

conclusionOur study elucidates that PDE5A is a novel direct target of miR-19a/b-3p, and demonstrates that antihypertrophic roles of the miR-19a/b-3p family in Ang II-induced hypertrophy and cardiac remodeling, suggests that endogenous miR-19a/b-3p might have clinical potential to suppress cardiac hypertrophy and heart failure.

Indexed as

Angiotensin IIAnimalsCardiomegalyCells, CulturedCyclic Nucleotide Phosphodiesterases, Type 5Gene Expression RegulationHumansHypertensionMice, TransgenicMicroRNAsMyocytes, CardiacSignal TransductionAngiotensin IICyclic Nucleotide Phosphodiesterases, Type 5MicroRNAsMIRN19A microRNA, humanMIRN19 microRNA, mousePde5a protein, mouse

Identifiers

PMID29664809
PMCPMC6080882
OpenAlexW2802920704

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.