We are analyzing https://link.springer.com/article/10.1007/s00018-023-04924-3.

Title:
Human myofibroblasts increase the arrhythmogenic potential of human induced pluripotent stem cell-derived cardiomyocytes | Cellular and Molecular Life Sciences
Description:
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have the potential to remuscularize infarcted hearts but their arrhythmogenicity remains an obstacle to safe transplantation. Myofibroblasts are the predominant cell-type in the infarcted myocardium but their impact on transplanted hiPSC-CMs remains poorly defined. Here, we investigate the effect of myofibroblasts on hiPSC-CMs electrophysiology and Ca2+ handling using optical mapping of advanced human cell coculture systems mimicking cell–cell interaction modalities. Human myofibroblasts altered the electrophysiology and Ca2+ handling of hiPSC-CMs and downregulated mRNAs encoding voltage channels (KV4.3, KV11.1 and Kir6.2) and SERCA2a calcium pump. Interleukin-6 was elevated in the presence of myofibroblasts and direct stimulation of hiPSC-CMs with exogenous interleukin-6 recapitulated the paracrine effects of myofibroblasts. Blocking interleukin-6 reduced the effects of myofibroblasts only in the absence of physical contact between cell-types. Myofibroblast-specific connexin43 knockdown reduced functional changes in contact cocultures only when combined with interleukin-6 blockade. This provides the first in-depth investigation into how human myofibroblasts modulate hiPSC-CMs function, identifying interleukin-6 and connexin43 as paracrine- and contact-mediators respectively, and highlighting their potential as targets for reducing arrhythmic risk in cardiac cell therapy.
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Keywords {🔍}

pubmed, myofbs, hipsccm, article, contact, google, scholar, fig, hipsccms, cardiac, control, human, cas, coculture, apd, cardiomyocytes, cells, decay, cell, central, medium, transient, stem, cocultures, noncontact, time, paracrine, mrna, myofibroblasts, fibroblasts, rate, conditioned, reduced, heart, culture, cultured, observed, potential, conditions, sirna, effect, handling, function, signalling, coupling, adult, treated, cxkd, interactions, monolayers,

Topics {✒️}

apc/cy7-conjugated cd31 antibody human ipsc-derived cardiomyocytes modulating esc/ipsc-cardiomyocyte electrophysiology utilising esc/ipsc-cardiomyocyte transplantation cardiac fibroblast-cardiomyocyte interactions alpha-smooth muscle actin purified ipsc-derived cardiomyocytes myofbs–hipsc-cms paracrine communication hipsc-cms transplant post-mi myofb-specific cx43-kd prevented interleukin-6-induced reciprocal expression article download pdf enhanced fibroblast–myocyte interactions heterotypic cell-cell coupling fluorescence-activated cell sorting combined myofb-specific cx43-kd transplanted human ipsc-cardiomyocytes hipsc-cm + cx43-kd myofbs short-range paracrine communication hipsc-cm + control kd myofbs embryonic stem cells sarcoplasmic reticulum ca2+-atpase langendorff-perfused mouse hearts cx43-based heterocellular coupling /bidirectional paracrine interactions pro-inflammatory cytokine produced acute myocardial infarction α-sma positive cells cell–cell interactions avoid immune-rejection [73] hipsc-cm electrical function redox-mediated reciprocal regulation hipsc-derived cardiomyocytes post-mi mouse hearts post-myocardial infarcted heart ongoing assail-mi trial clinical-grade hla haplobank therapeutic option post-mi transforming growth factor-β1 cardiac alternans induced myofb-specific cx43-kd hipsc-cm function similar human primate hearts na+-ca2+ exchanger contributes neutralising antibody prevented/reduced confluent hipsc-cm monolayers hipsc-cm molecular profile pure hipsc-cm cultures atrio-ventricular node conduction myofb-cardiomyocyte coupling contribute

Questions {❓}

Johnson RD, Camelliti P (2018) Role of non-myocyte gap junctions and connexin hemichannels in cardiovascular health and disease: novel therapeutic targets?

Schema {🗺️}

WebPage:
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         headline:Human myofibroblasts increase the arrhythmogenic potential of human induced pluripotent stem cell-derived cardiomyocytes
         description:Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have the potential to remuscularize infarcted hearts but their arrhythmogenicity remains an obstacle to safe transplantation. Myofibroblasts are the predominant cell-type in the infarcted myocardium but their impact on transplanted hiPSC-CMs remains poorly defined. Here, we investigate the effect of myofibroblasts on hiPSC-CMs electrophysiology and Ca2+ handling using optical mapping of advanced human cell coculture systems mimicking cell–cell interaction modalities. Human myofibroblasts altered the electrophysiology and Ca2+ handling of hiPSC-CMs and downregulated mRNAs encoding voltage channels (KV4.3, KV11.1 and Kir6.2) and SERCA2a calcium pump. Interleukin-6 was elevated in the presence of myofibroblasts and direct stimulation of hiPSC-CMs with exogenous interleukin-6 recapitulated the paracrine effects of myofibroblasts. Blocking interleukin-6 reduced the effects of myofibroblasts only in the absence of physical contact between cell-types. Myofibroblast-specific connexin43 knockdown reduced functional changes in contact cocultures only when combined with interleukin-6 blockade. This provides the first in-depth investigation into how human myofibroblasts modulate hiPSC-CMs function, identifying interleukin-6 and connexin43 as paracrine- and contact-mediators respectively, and highlighting their potential as targets for reducing arrhythmic risk in cardiac cell therapy.
         datePublished:2023-09-05T00:00:00Z
         dateModified:2024-12-27T00:00:00Z
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            Myocardial infarction
            Heterocellular communication
            Connexin-43
            Interleukin-6
            Fibroblasts
            Crosstalk
            Paracrine
            Cardiac fibroblast-cardiomyocyte interactions
            Crosstalk between cardiac fibroblasts and myocytes
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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ScholarlyArticle:
      headline:Human myofibroblasts increase the arrhythmogenic potential of human induced pluripotent stem cell-derived cardiomyocytes
      description:Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have the potential to remuscularize infarcted hearts but their arrhythmogenicity remains an obstacle to safe transplantation. Myofibroblasts are the predominant cell-type in the infarcted myocardium but their impact on transplanted hiPSC-CMs remains poorly defined. Here, we investigate the effect of myofibroblasts on hiPSC-CMs electrophysiology and Ca2+ handling using optical mapping of advanced human cell coculture systems mimicking cell–cell interaction modalities. Human myofibroblasts altered the electrophysiology and Ca2+ handling of hiPSC-CMs and downregulated mRNAs encoding voltage channels (KV4.3, KV11.1 and Kir6.2) and SERCA2a calcium pump. Interleukin-6 was elevated in the presence of myofibroblasts and direct stimulation of hiPSC-CMs with exogenous interleukin-6 recapitulated the paracrine effects of myofibroblasts. Blocking interleukin-6 reduced the effects of myofibroblasts only in the absence of physical contact between cell-types. Myofibroblast-specific connexin43 knockdown reduced functional changes in contact cocultures only when combined with interleukin-6 blockade. This provides the first in-depth investigation into how human myofibroblasts modulate hiPSC-CMs function, identifying interleukin-6 and connexin43 as paracrine- and contact-mediators respectively, and highlighting their potential as targets for reducing arrhythmic risk in cardiac cell therapy.
      datePublished:2023-09-05T00:00:00Z
      dateModified:2024-12-27T00:00:00Z
      pageStart:1
      pageEnd:18
      license:http://creativecommons.org/licenses/by/4.0/
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         Cardiac cell therapy
         Myocardial infarction
         Heterocellular communication
         Connexin-43
         Interleukin-6
         Fibroblasts
         Crosstalk
         Paracrine
         Cardiac fibroblast-cardiomyocyte interactions
         Crosstalk between cardiac fibroblasts and myocytes
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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         type:PostalAddress
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      name:Ming Lei
      affiliation:
            name:University of Oxford
            address:
               name:Department of Pharmacology, University of Oxford, Oxford, UK
               type:PostalAddress
            type:Organization
      name:John H. McVey
      url:http://orcid.org/0000-0002-7416-533X
      affiliation:
            name:University of Surrey
            address:
               name:School of Biosciences, University of Surrey, Guildford, UK
               type:PostalAddress
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