Evidence map›Paper›PMID 37656049›Full record

ArticleThe Journal of general physiology2023

Myosin expression and contractile function are altered by replating stem cell-derived cardiomyocytes.

Felix Osten, Natalie Weber, Meike Wendland, Tim Holler, Birgit Piep, Simon Kröhn, Jana Teske, Alea K Bodenschatz, Santoshi Biswanath Devadas, Kaja S Menge and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 2 countries.

Felix Osten *Institute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0001-5389-6056
Natalie Weber *Institute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0002-2302-1045
Meike WendlandInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0009-0005-3209-6507
Tim HollerInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0001-9981-7253
Birgit PiepInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0001-5505-9737
Simon KröhnInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0009-0008-8729-8001
Jana TeskeDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Hannover Medical School, Hannover, Germany.ORCID 0009-0000-4713-0900
Alea K BodenschatzInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0009-0001-4639-9454
Santoshi Biswanath DevadasDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Hannover Medical School, Hannover, Germany.ORCID 0000-0003-2887-0158
Kaja S MengeInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School , Hannover, Germany.ORCID 0009-0004-2711-1621
Shambhabi ChatterjeeInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School , Hannover, Germany.ORCID 0000-0001-5978-3562
Kristin SchwankeDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Hannover Medical School, Hannover, Germany.
Maike KosankeResearch Core Unit Genomics, Hannover Medical School , Hannover, Germany.ORCID 0000-0002-5910-2007
Judith MontagInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0002-4663-6966
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School , Hannover, Germany.ORCID 0000-0003-4360-1511
Robert ZweigerdtDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Hannover Medical School, Hannover, Germany.ORCID 0000-0002-4656-0770
Theresia KraftInstitute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0002-8386-8088
Bogdan Iorga *Institute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0000-0002-1000-8626
Joachim D Meissner *Institute of Molecular and Cell Physiology, Hannover Medical School , Hannover, Germany.ORCID 0009-0004-3253-8785
Medizinische Hochschule Hannover · DEUniversity of Bucharest · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myosin heavy chain (MyHC) is the main determinant of contractile function. Human ventricular cardiomyocytes (CMs) predominantly express the β-isoform. We previously demonstrated that ∼80% of human embryonic stem cell-derived cardiomyocytes (hESC-CMs) express exclusively β-MyHC after long-term culture on laminin-coated glass coverslips. Here, we investigated the impact of enzymatically detaching hESC-CMs after long-term culture and subsequently replating them for characterization of cellular function. We observed that force-related kinetic parameters, as measured in a micromechanical setup, resembled α- rather than β-MyHC-expressing myofibrils, as well as changes in calcium transients. Single-cell immunofluorescence analysis revealed that replating hESC-CMs led to rapid upregulation of α-MyHC, as indicated by increases in exclusively α-MyHC- and in mixed α/β-MyHC-expressing hESC-CMs. A comparable increase in heterogeneity of MyHC isoform expression was also found among individual human induced pluripotent stem cell (hiPSC)-derived CMs after replating. Changes in MyHC isoform expression and cardiomyocyte function induced by replating were reversible in the course of the second week after replating. Gene enrichment analysis based on RNA-sequencing data revealed changes in the expression profile of mechanosensation/-transduction-related genes and pathways, especially integrin-associated signaling. Accordingly, the integrin downstream mediator focal adhesion kinase (FAK) promoted β-MyHC expression on a stiff matrix, further validating gene enrichment analysis. To conclude, detachment and replating induced substantial changes in gene expression, MyHC isoform composition, and function of long-term cultivated human stem cell-derived CMs, thus inducing alterations in mechanosensation/-transduction, that need to be considered, particularly for downstream in vitro assays.

Indexed as

Induced Pluripotent Stem CellsMyocytes, CardiacHumansIntegrinsMyosin Heavy ChainsMyosinsIntegrinsMyosin Heavy ChainsMyosins

Identifiers

PMID37656049
PMCPMC10473967
OpenAlexW4386347849

What Socratic holds

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LicenceCC BY-NC-SA
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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 Socratic graph.