ArticleJournal of molecular and cellular cardiology2014
Acute slowing of cardiac conduction in response to myofibroblast coupling to cardiomyocytes through N-cadherin.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Vascularized Cardiac Tissue Engineering: From Advances in Biofabrication to Translational Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Essential role of obscurin kinase-1 in cardiomyocyte coupling via N-cadherin phosphorylation.JCI insight · 2024Article
- Opto-SICM framework combines optogenetics with scanning ion conductance microscopy for probing cell-to-cell contacts.Communications biology · 2023Article
- Cadherin-11-Interleukin-6 Signaling between Cardiac Fibroblast and Cardiomyocyte Promotes Ventricular Remodeling in a Mouse Pressure Overload-Induced Heart Failure Model.International journal of molecular sciences · 2023Article
- Active force generation contributes to the complexity of spontaneous activity and to the response to stretch of murine cardiomyocyte cultures.The Journal of physiology · 2022Article
- Changes in extracellular matrix in failing human non-ischemic and ischemic hearts with mechanical unloading.Journal of molecular and cellular cardiology · 2022Article
- Complex Relationship Between Cardiac Fibroblasts and Cardiomyocytes in Health and Disease.Journal of the American Heart Association · 2021Review
- Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells.Toxics · 2020Article
- Cadherin-11 blockade reduces inflammation-driven fibrotic remodeling and improves outcomes after myocardial infarction.JCI insight · 2019Article
- Cardiomyocyte-myofibroblast contact dynamism is modulated by connexin-43.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- ElectroMap: High-throughput open-source software for analysis and mapping of cardiac electrophysiology.Scientific reports · 2019Article
- Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.Basic research in cardiology · 2019Article
- Effect of Substrate Stiffness on Mechanical Coupling and Force Propagation at the Infarct Boundary.Biophysical journal · 2018Article
- Featured Article: TGF-β1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Mechanoregulation of Myofibroblast Fate and Cardiac Fibrosis.Advanced biosystems · 2018Article
- Mechanical signaling coordinates the embryonic heartbeat.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Atrial remodeling, fibrosis, and atrial fibrillation.Trends in cardiovascular medicine · 2015Review
- Mechanotransduction Mechanisms for Intraventricular Diastolic Vortex Forces and Myocardial Deformations: Part 2.Journal of cardiovascular translational research · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The electrophysiological consequences of cardiomyocyte and myofibroblast interactions remain unclear, and the contribution of mechanical coupling between these two cell types is still poorly understood. In this study, we examined the time course and mechanisms by which addition of myofibroblasts activated by transforming growth factor-beta (TGF-β) influence the conduction velocity (CV) of neonatal rat ventricular cell monolayers. We observed that myofibroblasts affected CV within 30 min of contact and that these effects were temporally correlated with membrane deformation of cardiomyocytes by the myofibroblasts. Expression of dominant negative RhoA in the myofibroblasts impaired both myofibroblast contraction and myofibroblast-induced slowing of cardiac conduction, whereas overexpression of constitutive RhoA had little effect. To determine the importance of mechanical coupling between these cell types, we examined the expression of the two primary cadherins in the heart (N- and OB-cadherin) at cell-cell contacts formed between myofibroblasts and cardiomyocytes. Although OB-cadherin was frequently found at myofibroblast-myofibroblast contacts, very little expression was observed at myofibroblast-cardiomyocyte contacts. The myofibroblast-induced slowing of cardiac conduction was not prevented by silencing of OB-cadherin in the myofibroblasts, and could be reversed by inhibitors of mechanosensitive channels (gadolinium or streptomycin) and cellular contraction (blebbistatin). In contrast, N-cadherin expression was commonly observed at myofibroblast-cardiomyocyte contacts, and silencing of N-cadherin in myofibroblasts prevented the myofibroblast-dependent slowing of cardiac conduction. We propose that myofibroblasts can impair the electrophysiological function of cardiac tissue through the application of contractile force to the cardiomyocyte membrane via N-cadherin junctions.
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Registered trials
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