Evidence map›Paper›PMID 30648591›Full record

ArticleJournal of food and drug analysis2019

Ubiquitin-protein ligase E3a (UBE3A) as a new biomarker of cardiac hypertrophy in cell models.

Kai-Chun Cheng, Yingxiao Li, Wei-Ting Chang, Zhih-Cherng Chen, Juei-Tang Cheng, Cheng-Chia Tsai

Open access · hybridAbstract read
In one paragraph

Article in Journal of food and drug analysis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 15 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 3 institutions in 2 countries.

Kai-Chun ChengDepartment of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890, Japan.
Yingxiao LiDepartment of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890, Japan.
Wei-Ting ChangDepartment of Cardiology, Chi-Mei Medical Center, Yong Kang, Tainan City, 71003, Taiwan.
Zhih-Cherng ChenDepartment of Cardiology, Chi-Mei Medical Center, Yong Kang, Tainan City, 71003, Taiwan.
Juei-Tang ChengDepartment of Medical Research, Chi-Mei Medical Center, Yong Kang, Tainan City, 71003, Taiwan.
Cheng-Chia TsaiDepartment of Surgery, Mackay Memorial Hospital, Mackay Medical University, Taipei City, 25245, Taiwan.
Chi Mei Medical Center · TWKagoshima University · JPMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is widely diagnosed in clinical cardiac disorders. The pathophysiology of hypertrophy is complex and multifactorial, a series of molecular and cellular changes are participated, such as activation of different signaling pathways, a switch of fetal gene program in the myocardium, and apoptosis. Some biomarkers have been applied to assess cardiac hypertrophy including atrial natriuretic peptides (ANP), brain/B-type natriuretic peptides (BNP), and α- or β- Myosin Heavy Chain (MHC) in addition to others. Recently, ubiquitin-protein ligase E3A (UBE3A) has been observed to increase in cardiac hypertrophy. Therefore, UBE3A as a new biomarker seems valuable in the clinic. The cardiac hypertrophy is induced in rat-derived heart cell line H9c2 cells by potassium bromate (KBrO3), high glucose (HG), or isoproterenol (Iso), respectively. As an oxidizing agent, KBrO3 increased cell size at concentrations less than 250 μM. Similarly, HG and Iso also induced cardiac hypertrophy in H9c2 cells. Interestingly, each kind of the cell models promoted the gene expression of the well-known biomarkers of cardiac hypertrophy including atrial natriuretic peptides (ANP) and brain/B-type natriuretic peptides (BNP). Additionally, UBE3A is also raised with the signals involved in cardiac hypertrophy such as calcineurin and nuclear factor of activated T-cells (NFAT) determined using Western blots. KBrO3 increased the protein levels of these signals and the specific inhibitor, such as cyclosporine A and tacrolimus, attenuated the signaling in H9c2 cells at concentrations sufficient to inhibit calcineurin in addition to the reduction of mRNA levels of UBE3A, similar to ANP or BNP. Moreover, HG or Iso also significantly increased protein levels of UBE3A in H9c2 cells. Taken together, we provided a new view that UBE3A is markedly raised in cardiac hypertrophy using various cell models, mainly through the activation of the calcineurin/NFAT signaling pathway in H9c2 cells. Therefore, UBE3A could be developed as a new biomarker in the diagnosis of cardiac hypertrophy.

Indexed as

AnimalsAtrial Natriuretic FactorBiomarkersCalcineurinCardiomegalyCell LineHumansModels, BiologicalMyocytes, CardiacNatriuretic Peptide, BrainNFATC Transcription FactorsRatsUbiquitin-Protein LigasesAtrial Natriuretic FactorBiomarkersCalcineurinNatriuretic Peptide, BrainNFATC Transcription FactorsUbe3a protein, ratUbiquitin-Protein LigasesH9c2 cellsHyperglycemiaHypertrophic signalsIsoproterenolPotassium bromate

Identifiers

PMID30648591
PMCPMC9298619
OpenAlexW2888344501

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LicenceCC BY-NC-ND
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Registered trials

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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.