Evidence map›Paper›PMID 22219180›Full record

ArticleCardiovascular research2012

GATA4 expression is primarily regulated via a miR-26b-dependent post-transcriptional mechanism during cardiac hypertrophy.

Mingyue Han, Zhi Yang, Danish Sayed, Minzhen He, Shumin Gao, Lin Lin, Seonghun Yoon, Maha Abdellatif

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

Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  8. MicroRNAs: The Missing Link between Hypertension and Periodontitis?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

8 authors at 1 institution in 1 country.

Mingyue HanDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.
Zhi Yang
Danish Sayed
Minzhen He
Shumin Gao
Lin Lin
Seonghun Yoon
Maha Abdellatif
New Jersey Institute of Technology · US

Funding

Mechanisms of RasGAP in cardiac cell growth and survivalR01HL057970 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 2004 to 2014
$2.8M
The role of microRNA in cardiac cell deathR01HL104115 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 2010 to 2014
$1.6M
RAS DEPENDENT SIGNALING IN CARDIAC HYPERTROPHYR29HL057970 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 1998 to 2002
$297k
NHLBI NIH HHS HL057970NHLBI NIH HHS HL104115
6 · The paper itself

Abstract

aimsGATA4 is a transcription factor that is up-regulated during cardiac hypertrophy and plays a fundamental role in myocyte growth and survival. In this study, we investigate the transcriptional vs. post-transcriptional mechanisms that are involved in regulating GATA4 in the heart during neonatal and pressure overload-induced hypertrophic growth. METHODS AND

resultsGATA4 protein is significantly higher during pressure overload-induced (2.9 ± 0.4-fold) and neonatal (6.8 ± 1-fold) hypertrophic growth vs. the normal adult mouse heart. Using RNA polymerase II immunoprecipitation combined with deep sequencing, we confirmed that active transcription of the Gata4 gene remained unchanged during hypertrophy, whereas it was two-fold higher in the neonatal vs. adult heart, commensurate with the mRNA levels. These results suggested a post-transcriptional mode of regulation of its expression, which prompted the identification of a conserved sequence in its 3'-untranslated region that was responsible for reduced translation via miR-26b. Overexpression of miR-26b reduced GATA4-dependent transcription, endothelin-induced hypertrophy, and sensitized the cells to apoptotic insults. Additionally, miR-26b targeted phospholipase C-β1, which, in turn, inhibited miR-26b expression, creating a double-negative feedback loop. Accordingly, overexpression of miR-26b in the heart inhibited up-regulation of its targets and the development of hypertrophy. However, knockdown of miR-26b is not sufficient for inducing hypertrophy.

conclusionDown-regulation of miR-26b in the heart is required for the up-regulation of GATA4 and the induction of pressure-induced cardiac hypertrophy. The results also underscore the functional relevance of miRNAs in regulating gene expression during cardiac hypertrophy.

Indexed as

AnimalsCardiomegalyDisease Models, AnimalDown-RegulationGATA4 Transcription FactorGene Expression RegulationMiceMice, Inbred C57BLMice, TransgenicMicroRNAsPhospholipase C betaRNA Processing, Post-TranscriptionalTranscription, GeneticUp-RegulationGata4 protein, mouseGATA4 Transcription FactorMicroRNAsMirn26 microRNA, mousePhospholipase C beta

Identifiers

PMID22219180
PMCPMC3291090
OpenAlexW1969050423

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.