ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Prolonged mechanical unloading affects cardiomyocyte excitation-contraction coupling, transverse-tubule structure, and the cell surface.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Cardiac unloading models for myocardial reverse remodeling.Basic research in cardiology · 2026Review
- A Correlative SICM-OPM Platform for Surface and Volumetric Imaging in Live Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- T-tubular remodeling occurs in a cardiomyocyte-autonomous manner following pathological mechanical stiffness exposure.Journal of molecular and cellular cardiology plus · 2026Article
- Active Colitis Attenuates Ventricular Excitation-Contraction Coupling by T-Tubular Remodeling.Biomolecules · 2026Article
- Stress-Induced calcium mishandling in cardiac (Patho)physiology.Cellular and molecular life sciences : CMLS · 2025Review
- Cellular shortening and calcium dynamics are improved by noisy stimulus in a model of cardiomyopathy.Scientific reports · 2023Article
- Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023Article
- Cardiac mechanics and reverse remodelling under mechanical support from left ventricular assist devices.Frontiers in cardiovascular medicine · 2023Review
- Serial block face scanning electron microscopy reveals region-dependent remodelling of transverse tubules post-myocardial infarction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- A practical guide for investigating cardiac physiology using living myocardial slices.Basic research in cardiology · 2020Review
- Nexilin Is Necessary for Maintaining the Transverse-Axial Tubular System in Adult Cardiomyocytes.Circulation. Heart failure · 2020Article
- Myocardial slices come to age: an intermediate complexity in vitro cardiac model for translational research.Cardiovascular research · 2020Review
- Biomimetic electromechanical stimulation to maintain adult myocardial slices in vitro.Nature communications · 2019Article
- Cardiomyocyte substructure reverts to an immature phenotype during heart failure.The Journal of physiology · 2019Article
- The Development of Compartmentation of cAMP Signaling in Cardiomyocytes: The Role of T-Tubules and Caveolae Microdomains.Journal of cardiovascular development and disease · 2018Review
- Caveolin 3-dependent loss of t-tubular IExperimental physiology · 2018Article
- Partial Mechanical Unloading of the Heart Disrupts L-Type Calcium Channel and Beta-Adrenoceptor Signaling Microdomains.Frontiers in physiology · 2018Article
- Transverse tubule remodelling: a cellular pathology driven by both sides of the plasmalemma?Biophysical reviews · 2017Review
- Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Current heart failure reports · 2017Review
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10 authors.
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Abstract
Prolonged mechanical unloading (UN) of the heart is associated with detrimental changes to the structure and function of cardiomyocytes. The mechanisms underlying these changes are unknown. In this study, we report the influence of UN on excitation-contraction coupling, Ca(2+)-induced Ca(2+) release (CICR) in particular, and transverse (t)-tubule structure. UN was induced in male Lewis rat hearts by heterotopic abdominal heart transplantation. Left ventricular cardiomyocytes were isolated from the transplanted hearts after 4 wk and studied using whole-cell patch clamping, confocal microscopy, and scanning ion conductance microscopy (SICM). Recipient hearts were used as control (C). UN reduced the volume of cardiomyocytes by 56.5% compared with C (UN, n=90; C, n=59; P<0.001). The variance of time-to-peak of the Ca(2+) transients was significantly increased in unloaded cardiomyocytes (UN 227.4+/-24.9 ms(2), n=42 vs. C 157.8+/-18.0 ms(2), n=40; P<0.05). UN did not alter the action potential morphology or whole-cell L-type Ca(2+) current compared with C, but caused a significantly higher Ca(2+) spark frequency (UN 3.718+/-0.85 events/100 mum/s, n=47 vs. C 0.908+/-0.186 events/100 microm/s, n=45; P<0.05). Confocal studies showed irregular distribution of the t tubules (power of the normal t-tubule frequency: UN 8.13+/-1.12x10(5), n=57 vs. C 20.60+/- 3.174x10(5), n=56; P<0.001) and SICM studies revealed a profound disruption to the openings of the t tubules and the cell surface in unloaded cardiomyocytes. We show that UN leads to a functional uncoupling of the CICR process and identify disruption of the t-tubule-sarcoplasmic reticulum interaction as a possible mechanism.
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