Evidence map›Paper›PMID 31991811›Full record

ArticleCells2020

Anti-CD3 Antibody Treatment Reduces Scar Formation in a Rat Model of Myocardial Infarction.

Bernhard Wernly, Vera Paar, Achim Aigner, Patrick M Pilz, Bruno K Podesser, Martin Förster, Christian Jung, Josefina Pinon Hofbauer, Birgit Tockner, Monika Wimmer and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 18 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

16 authors at 6 institutions in 3 countries.

Bernhard WernlyDepartment of Internal Medicine II, Division of Cardiology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Vera PaarDepartment of Internal Medicine II, Division of Cardiology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Achim AignerRudolf Boehm-Institute for Pharmacology and Toxicology, Clinical Pharmacology, Leipzig University, Faculty of Medicine, 04107 Leipzig, Germany.
Patrick M PilzLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University Vienna, 1080 Vienna, Austria.
Bruno K PodesserLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University Vienna, 1080 Vienna, Austria.
Martin FörsterUniversitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University, Jena 07743, Germany.
Christian JungDivision of Cardiology, Pulmonology, and Vascular Medicine University Duesseldorf, Medical Faculty, 40225 Duesseldorf, Germany.
Josefina Pinon HofbauerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology and Allergology, University Hospital of the Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Birgit TocknerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology and Allergology, University Hospital of the Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Monika WimmerEB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology and Allergology, University Hospital of the Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Theo KrausDepartment of Pathology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Lukas J MotlochDepartment of Internal Medicine II, Division of Cardiology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Matthias HacklTAmiRNA GmbH, Leberstrasse 20, 1110 Vienna, Austria.
Uta C HoppeDepartment of Internal Medicine II, Division of Cardiology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Attila KissLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University Vienna, 1080 Vienna, Austria.
Michael LichtenauerDepartment of Internal Medicine II, Division of Cardiology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.
Paracelsus Medical University · ATLudwig Boltzmann Institute for Digital Health and Prevention · ATFriedrich Schiller University Jena · DEHeinrich Heine University Düsseldorf · DEKarolinska University Hospital · SELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

methodsConcentrations of IL-8 and MCP-1 in supernatants of human peripheral blood mononuclear cell (PBMC) cultures following distinct antibody treatments were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). In vivo, anti-CD3 antibodies or vehicle were injected intravenously in rats subjected to acute myocardial infarction (AMI). Chemotaxis and angiogenesis were evaluated using tube and migration assays. Intracellular pathways were assessed using Western blot. Extracellular vesicles (EVs) were quantitatively evaluated using fluorescence-activated cell scanning, exoELISA, and nanoparticle tracking analysis. Also, microRNA profiles were determined by next-generation sequencing.

resultsOnly PBMC stimulation with anti-CD3 antibody led to IL-8 and MCP-1 changes in secretion, similar to ATG. In a rat model of AMI, systemic treatment with an anti-CD3 antibody markedly reduced infarct scar size (27.8% (Inter-quartile range; IQR 16.2-34.9) vs. 12.6% (IQR 8.3-27.2);

conclusionTreatment with an anti-CD3 antibody led to decreased scar size in a rat model of AMI. Whereas cardioprotective and pro-angiogenetic pathways were unaltered by anti-CD3 treatment, qualitative changes in the EVs miRNA expression could be observed, which might be causal for the observed cardioprotective phenotype. We provide evidence that EVs are a potential cardioprotective treatment target. Our findings will also provide the basis for a more detailed analysis of putatively relevant miRNA candidates.

Indexed as

AnimalsAntibodiesAntilymphocyte SerumCardiotonic AgentsCD3 ComplexChemokine CCL2CicatrixDisease Models, AnimalExosomesExtracellular VesiclesHigh-Throughput Nucleotide SequencingHumansHuman Umbilical Vein Endothelial CellsInterleukin-8Leukocytes, MononuclearMaleAntibodiesAntilymphocyte SerumCardiotonic AgentsCCL2 protein, humanCD3 ComplexChemokine CCL2Interleukin-8MicroRNAsProteomeAMIangiogenesisantibody treatmentanti-CDapoptosiscardioprotectionCD3miRNAmyocardial infarction

Identifiers

PMID31991811
PMCPMC7072364
OpenAlexW3002083338

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.