Evidence map›Paper›PMID 32077168›Full record

ArticleCell proliferation2020

Aberrant expression of miR-29b-3p influences heart development and cardiomyocyte proliferation by targeting NOTCH2.

Qian Yang, Fang Wu, Yaping Mi, Feng Wang, Ke Cai, Xiaoshan Yang, Ranran Zhang, Lian Liu, Yawen Zhang, Youhua Wang and 4 more

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

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
3.5field-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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
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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

14 authors at 5 institutions in 1 country.

Qian YangTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-9493-6381
Fang WuTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.
Yaping MiCardiovascular Center, Children's Hospital of Fudan University, Shanghai, China.
Feng WangTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.
Ke CaiCardiovascular Center, Children's Hospital of Fudan University, Shanghai, China.
Xiaoshan YangDepartment of Bioscience, Bengbu Medical College, Bengbu, China.
Ranran ZhangCardiovascular Center, Children's Hospital of Fudan University, Shanghai, China.
Lian LiuCardiovascular Center, Children's Hospital of Fudan University, Shanghai, China.
Yawen ZhangTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.
Youhua WangLonghua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Xu WangCancer Metabolism Laboratory, Cancer Institute, Fudan University, Shanghai, China.
Mingqing XuBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-3473-5748
Yonghao GuiTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.
Qiang LiTranslational Medical Center for Development and Disease, Institute of Pediatrics, Shanghai Key Laboratory of Birth Defect, Children's Hospital of Fudan University, Shanghai, China.
Children's Hospital of Fudan University · CNBengbu Medical College · CNFudan University Shanghai Cancer Center · CNShanghai Jiao Tong University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

973 Program 2013CB945401National Key Research and Development Program 2016YFC1000500National Natural Science Foundations of China 81170147National Natural Science Foundations of China 81470442National Natural Science Foundations of China 81741081National Natural Science Foundations of China 81771632National Natural Science Foundations of China 81873481Shanghai Key Laboratory of Birth Defect 13DZ2260600Shanghai Municipal Commission of Science and Technology Program 13JC1403700Shanghai Municipal Education Commission ZXDF089002
6 · The paper itself

Abstract

objectivesmicroRNA-29 (miR-29) family have shown different expression patterns in cardiovascular diseases. Our study aims to explore the effect and mechanism of miR-29 family on cardiac development. MATERIALS AND

methodsA total of 13 patients with congenital heart disease (CHD) and 7 controls were included in our study. Tissues were obtained from the right ventricular outflow tract (RVOT) after surgical resection or autopsy. The next-generation sequencing was applied to screen the microRNA expression profiles of CHD. Quantitative RT-PCR and Western blot were employed to measure genes expression. Tg Cmlc2: GFP reporter zebrafish embryos were injected with microRNA (miRNA) to explore its role in cardiac development in vivo. Dual-luciferase reporter assay was designed to validate the target gene of miRNAs. CCK-8 and EdU incorporation assays were performed to evaluate cardiomyocyte proliferation.

resultsOur study showed miR-29b-3p expression was significantly increased in the RVOT of the CHD patients. Injection of miR-29b-3p into zebrafish embryos induced higher mortality and malformation rates, developmental delay, cardiac malformation and dysfunction. miR-29b-3p inhibited cardiomyocyte proliferation, and its inhibitor promoted cardiomyocyte proliferation in vitro and in vivo. Furthermore, we identified that miR-29b-3p influenced cardiomyocyte proliferation by targeting NOTCH2, which was down-regulated in the RVOT of the CHD patients.

conclusionThis study reveals that miR-29b-3p functions as a novel regulator of cardiac development and inhibits cardiomyocyte proliferation via NOTCH2, which provides novel insights into the aetiology and potential treatment of CHD.

Indexed as

AnimalsCell ProliferationCells, CulturedChild, PreschoolDown-RegulationFemaleHeartHeart Defects, CongenitalHumansInfantMaleMiceMicroRNAsMyocytes, CardiacReceptor, Notch2Up-RegulationMicroRNAsMIRN29a microRNA, humanNOTCH2 protein, humanReceptor, Notch2congenital heart diseasemicroRNA-29b-3pNOTCH2proliferation

Identifiers

PMID32077168
PMCPMC7106969
OpenAlexW3008322994

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.