Evidence map›Paper›PMID 37686171›Full record

ArticleInternational journal of molecular sciences2023

Knockout of the Cardiac Transcription Factor NKX2-5 Results in Stem Cell-Derived Cardiac Cells with Typical Purkinje Cell-like Signal Transduction and Extracellular Matrix Formation.

Paul Disse, Isabel Aymanns, Lena Mücher, Sarah Sandmann, Julian Varghese, Nadine Ritter, Nathalie Strutz-Seebohm, Guiscard Seebohm, Stefan Peischard

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Editorial: Transcriptional regulation in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024
    Article
  3. Heart rhythmFrontiers in cardiovascular medicine · 2024
    Article
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

9 authors at 2 institutions in 1 country.

Paul DisseInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.ORCID 0000-0003-1566-5016
Isabel AymannsInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.
Lena MücherInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.
Sarah SandmannInstitute of Medical Informatics, University of Münster, D-48149 Münster, Germany.ORCID 0000-0002-5011-0641
Julian VargheseInstitute of Medical Informatics, University of Münster, D-48149 Münster, Germany.ORCID 0000-0002-7206-3719
Nadine RitterInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.ORCID 0000-0003-2749-885X
Nathalie Strutz-SeebohmInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.
Guiscard SeebohmInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.
Stefan PeischardInstitute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany.
University Hospital Münster · DEUniversity of Münster · DE

Funding

Deutsche Forschungsgemeinschaft FOR 5146Deutsche Forschungsgemeinschaft GRK 2515Deutsche Forschungsgemeinschaft Se1077/13-1
6 · The paper itself

Abstract

The human heart controls blood flow, and therewith enables the adequate supply of oxygen and nutrients to the body. The correct function of the heart is coordinated by the interplay of different cardiac cell types. Thereby, one can distinguish between cells of the working myocardium, the pace-making cells in the sinoatrial node (SAN) and the conduction system cells in the AV-node, the His-bundle or the Purkinje fibres. Tissue-engineering approaches aim to generate hiPSC-derived cardiac tissues for disease modelling and therapeutic usage with a significant improvement in the differentiation quality of myocardium and pace-making cells. The differentiation of cells with cardiac conduction system properties is still challenging, and the produced cell mass and quality is poor. Here, we describe the generation of cardiac cells with properties of the cardiac conduction system, called conduction system-like cells (CSLC). As a primary approach, we introduced a CrispR-Cas9-directed knockout of the NKX2-5 gene in hiPSC. NKX2-5-deficient hiPSC showed altered connexin expression patterns characteristic for the cardiac conduction system with strong connexin 40 and connexin 43 expression and suppressed connexin 45 expression. Application of differentiation protocols for ventricular- or SAN-like cells could not reverse this connexin expression pattern, indicating a stable regulation by NKX2-5 on connexin expression. The contraction behaviour of the hiPSC-derived CSLCs was compared to hiPSC-derived ventricular- and SAN-like cells. We found that the contraction speed of CSLCs resembled the expected contraction rate of human conduction system cells. Overall contraction was reduced in differentiated cells derived from NKX2-5 knockout hiPSC. Comparative transcriptomic data suggest a specification of the cardiac subtype of CSLC that is distinctly different from ventricular or pacemaker-like cells with reduced myocardial gene expression and enhanced extracellular matrix formation for improved electrical insulation. In summary, knockout of NKX2-5 in hiPSC leads to enhanced differentiation of cells with cardiac conduction system features, including connexin expression and contraction behaviour.

Indexed as

Homeobox Protein Nkx-2.5Purkinje CellsTranscription FactorsCardiac Conduction System DiseaseHumansInduced Pluripotent Stem CellsPurkinje FibersSignal TransductionSinoatrial NodeStem CellsHomeobox Protein Nkx-2.5NKX2-5 protein, humanTranscription Factorscardiac conduction systemcollagenconnexinCrispR-Cas9hiPSCNKX2-5

Identifiers

PMID37686171
PMCPMC10487652
OpenAlexW4386251142

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.