Evidence map›Paper›PMID 21149577›Full record

ArticleMolecular and cellular biology2011

MicroRNA-27a regulates beta cardiac myosin heavy chain gene expression by targeting thyroid hormone receptor beta1 in neonatal rat ventricular myocytes.

Hitoo Nishi, Koh Ono, Takahiro Horie, Kazuya Nagao, Minako Kinoshita, Yasuhide Kuwabara, Shin Watanabe, Tomohide Takaya, Yodo Tamaki, Rieko Takanabe-Mori and 6 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Article
  8. Epigenetic Regulation of Autophagy in Cardiovascular Pathobiology.International journal of molecular sciences · 2021
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  10. Aging, MicroRNAs, and Heart Failure.Current problems in cardiology · 2020
    Review
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  13. Article
  14. Article
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  16. Article
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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

16 authors at 3 institutions in 1 country.

Hitoo NishiDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Koh Ono
Takahiro Horie
Kazuya Nagao
Minako Kinoshita
Yasuhide Kuwabara
Shin Watanabe
Tomohide Takaya
Yodo Tamaki
Rieko Takanabe-Mori
Hiromichi Wada
Koji Hasegawa
Yoshitaka Iwanaga
Teruhisa Kawamura
Toru Kita
Takeshi Kimura
Kyoto University · JPKyoto Medical Center · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs), small noncoding RNAs, are negative regulators of gene expression and play important roles in gene regulation in the heart. To examine the role of miRNAs in the expression of the two isoforms of the cardiac myosin heavy chain (MHC) gene, α- and β-MHC, which regulate cardiac contractility, endogenous miRNAs were downregulated in neonatal rat ventricular myocytes (NRVMs) using lentivirus-mediated small interfering RNA (siRNA) against Dicer, an essential enzyme for miRNA biosynthesis, and MHC expression levels were examined. As a result, Dicer siRNA could downregulate endogenous miRNAs simultaneously and the β-MHC gene but not α-MHC, which implied that specific miRNAs could upregulate the β-MHC gene. Among 19 selected miRNAs, miR-27a was found to most strongly upregulate the β-MHC gene but not α-MHC. Moreover, β-MHC protein was downregulated by silencing of endogenous miR-27a. Through a bioinformatics screening using TargetScan, we identified thyroid hormone receptor β1 (TRβ1), which negatively regulates β-MHC transcription, as a target of miR-27a. Moreover, miR-27a was demonstrated to modulate β-MHC gene regulation via thyroid hormone signaling and to be upregulated during the differentiation of mouse embryonic stem (ES) cells or in hypertrophic hearts in association with β-MHC gene upregulation. These findings suggested that miR-27a regulates β-MHC gene expression by targeting TRβ1 in cardiomyocytes.

Indexed as

AnimalsAnimals, NewbornBase SequenceCell DifferentiationDNA PrimersEmbryonic Stem CellsGene Expression RegulationHeart VentriclesIn Vitro TechniquesMaleMiceMice, Inbred C57BLMice, Inbred ICRMicroRNAsMyocytes, CardiacMyosin Heavy ChainsDNA PrimersMicroRNAsMirn27 microRNA, mouseMyh7 protein, mouseMYH7 protein, ratMyosin Heavy ChainsRibonuclease IIIRNA, Small InterferingThyroid Hormone Receptors beta

Identifiers

PMID21149577
PMCPMC3028640
OpenAlexW2097633891

What OpenQuestion 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 OpenQuestion graph.