Evidence map›Paper›PMID 22174827›Full record

ArticlePloS one2011

Human cardiac-derived adherent proliferating cells reduce murine acute Coxsackievirus B3-induced myocarditis.

Kapka Miteva, Marion Haag, Jun Peng, Kostas Savvatis, Peter Moritz Becher, Martina Seifert, Katrin Warstat, Dirk Westermann, Jochen Ringe, Michael Sittinger and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  4. A Toolbox of Potential Immune-Related Therapies for Inflammatory Cardiomyopathy.Journal of cardiovascular translational research · 2021
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  17. Regulatory T cells in cardiovascular diseases.Nature reviews. Cardiology · 2016
    Review
  18. Article
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  20. Review
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

13 authors at 3 institutions in 2 countries.

Kapka MitevaBerlin-Brandenburg Center for Regenerative Therapies, Charité, University Medicine Berlin, Campus Virchow, Berlin, Germany.
Marion Haag
Jun Peng
Kostas Savvatis
Peter Moritz Becher
Martina Seifert
Katrin Warstat
Dirk Westermann
Jochen Ringe
Michael Sittinger
Heinz-Peter Schultheiss
Carsten Tschöpe
Sophie Van Linthout
Charité - Universitätsmedizin Berlin · DEBerlin-Brandenburger Centrum für Regenerative Therapien · DEFranklin University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnder conventional heart failure therapy, inflammatory cardiomyopathy typically has a progressive course, indicating a need for alternative therapeutic strategies to improve long-term outcomes. We recently isolated and identified novel cardiac-derived cells from human cardiac biopsies: cardiac-derived adherent proliferating cells (CAPs). They have similarities with mesenchymal stromal cells, which are known for their anti-apoptotic and immunomodulatory properties. We explored whether CAPs application could be a novel strategy to improve acute Coxsackievirus B3 (CVB3)-induced myocarditis. METHODOLOGY/PRINCIPAL

findingsTo evaluate the safety of our approach, we first analyzed the expression of the coxsackie- and adenovirus receptor (CAR) and the co-receptor CD55 on CAPs, which are both required for effective CVB3 infectivity. We could demonstrate that CAPs only minimally express both receptors, which translates to minimal CVB3 copy numbers, and without viral particle release after CVB3 infection. Co-culture of CAPs with CVB3-infected HL-1 cardiomyocytes resulted in a reduction of CVB3-induced HL-1 apoptosis and viral progeny release. In addition, CAPs reduced CD4 and CD8 T cell proliferation. All CAPs-mediated protective effects were nitric oxide- and interleukin-10-dependent and required interferon-γ. In an acute murine model of CVB3-induced myocarditis, application of CAPs led to a decrease of cardiac apoptosis, cardiac CVB3 viral load and improved left ventricular contractility parameters. This was associated with a decline in cardiac mononuclear cell activity, an increase in T regulatory cells and T cell apoptosis, and an increase in left ventricular interleukin-10 and interferon-γ mRNA expression.

conclusionsWe conclude that CAPs are a unique type of cardiac-derived cells and promising tools to improve acute CVB3-induced myocarditis.

Indexed as

AnimalsApoptosisCD55 AntigensCell AdhesionCell ProliferationCell SurvivalCell TransplantationCoxsackie and Adenovirus Receptor-Like Membrane ProteinCoxsackievirus InfectionsEnterovirusHumansImmunomodulationInjections, IntravenousInterferon-gammaInterleukin-10MiceCD55 AntigensCLMP protein, humanCLMP protein, mouseCoxsackie and Adenovirus Receptor-Like Membrane ProteinInterferon-gammaInterleukin-10Nitric OxideReceptors, Virus

Identifiers

PMID22174827
PMCPMC3235117
OpenAlexW2109233468

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.