Evidence map›Paper›PMID 26264759›Full record

ArticleJournal of molecular and cellular cardiology2015

Acetylation mediates Cx43 reduction caused by electrical stimulation.

Viviana Meraviglia, Valerio Azzimato, Claudia Colussi, Maria Cristina Florio, Anna Binda, Alice Panariti, Khaled Qanud, Silvia Suffredini, Laura Gennaccaro, Michele Miragoli and 9 more

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 17 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

19 authors at 12 institutions in 3 countries.

Viviana MeravigliaLaboratory of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, Milano, Italy; Center for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy.
Valerio AzzimatoLaboratory of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, Milano, Italy; Department of Pharmacology, Chemotherapy and Medical Toxicology, Università degli Studi di Milano, Milano, Italy.
Claudia ColussiIstituto di Patologia Medica, Università Cattolica del SacroCuore, Roma, Italy.
Maria Cristina FlorioCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy.
Anna BindaDepartment of Health Science, University of Milano Bicocca, Monza, Italy.
Alice PanaritiDepartment of Health Science, University of Milano Bicocca, Monza, Italy.
Khaled QanudDepartment of Physiology, New York Medical College, Valhalla, NY, United States.
Silvia SuffrediniCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy.
Laura GennaccaroCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy; Department of Life Sciences, University of Parma, Parma, Italy.
Michele MiragoliCERT, Center of Excellence for Toxicological Research, INAIL, ex ISPESL, University of Parma, Parma, Italy; Humanitas Clinical and Research Center, Rozzano Milano, Italy.
Andrea BarbutiThe PaceLab, Department of Biosciences, Università di Milano, Italy.
Paul D LampeTranslational Research Program, Fred Hutchinson Cancer Research Center, Seattle, WA, United States.
Carlo GaetanoDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, Germany.
Peter P PramstallerCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy.
Maurizio C CapogrossiLaboratory of Vascular Pathology, Istituto Dermopatico dell'Immacolata IRCCS, Roma, Italy.
Fabio A RecchiaDepartment of Physiology, Temple University School of Medicine, Philadelphia, PA, United States; Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Giulio PompilioLaboratory of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, Milano, Italy; Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milano, Italy.
Ilaria RivoltaDepartment of Health Science, University of Milano Bicocca, Monza, Italy.
Alessandra RossiniCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy. Electronic address: alessandra.rossini@eurac.edu.
Eurac Research · ITUniversity of Milano-Bicocca · ITCentro Cardiologico Monzino · ITUniversity of Parma · ITFred Hutch Cancer Center · USGoethe University Frankfurt · DEIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto Dermopatico dell'Immacolata · ITNew York Medical College · USScuola Superiore Sant'Anna · ITUniversità Cattolica del Sacro Cuore · ITUniversity of Milan · IT

Funding

Substrate Selection and Oxidative Stress in Heart FailureP01HL074237 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2003 to 2013
$19.9M
PHOSPHORYLATION OF GAP JUNCTION PROTEINSR01GM055632 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LAMPE, PAUL D. · 1997 to 2017
$6.1M
VEGF receptor-1-mediated protection in dilated cardiomyopathyR01HL108213 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RECCHIA, FABIO A · 2012 to 2015
$1.6M
NHLBI NIH HHS P01 HL074237NHLBI NIH HHS P01 HL-74237NHLBI NIH HHS R01 HL-108213NHLBI NIH HHS R01 HL108213NIGMS NIH HHS R01 GM055632
6 · The paper itself

Abstract

Communication between cardiomyocytes depends upon gap junctions (GJ). Previous studies have demonstrated that electrical stimulation induces GJ remodeling and modifies histone acetylase (HAT) and deacetylase (HDAC) activities, although these two results have not been linked. The aim of this work was to establish whether electrical stimulation modulates GJ-mediated cardiac cell-cell communication by acetylation-dependent mechanisms. Field stimulation of HL-1 cardiomyocytes at 0.5 Hz for 24 h significantly reduced connexin43 (Cx43) expression and cell-cell communication. HDAC activity was down-regulated whereas HAT activity was not modified resulting in increased acetylation of Cx43. Consistent with a post-translational mechanism, we did not observe a reduction in Cx43 mRNA in electrically stimulated cells, while the proteasomal inhibitor MG132 maintained Cx43 expression. Further, the treatment of paced cells with the HAT inhibitor Anacardic Acid maintained both the levels of Cx43 and cell-cell communication. Finally, we observed increased acetylation of Cx43 in the left ventricles of dogs subjected to chronic tachypacing as a model of abnormal ventricular activation. In conclusion, our findings suggest that altered electrical activity can regulate cardiomyocyte communication by influencing the acetylation status of Cx43.

Indexed as

AcetylationAnacardic AcidsAnimalsCell CommunicationConnexin 43DogsElectric StimulationGap JunctionsHeart VentriclesHistone AcetyltransferasesHistone Deacetylase 1HumansMiceMyocytes, CardiacRNA, Messengeranacardic acidAnacardic AcidsConnexin 43Hdac1 protein, mouseHistone AcetyltransferasesHistone Deacetylase 1RNA, MessengerAcetylationConnexin43Electrical field stimulationGap junctions

Identifiers

PMID26264759
PMCPMC4637213
OpenAlexW1917470978

What OpenQuestion holds

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LicenceTDM
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.