ArticleThe Journal of physiology2007
Role of myosin heavy chain composition in the stretch activation response of rat myocardium.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- A Drosophila cardiac myosin increases jump muscle stretch activation and shortening deactivation.Biophysical journal · 2025Article
- Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022Article
- Cellular Phenotypic Transformation in Heart Failure Caused by Coronary Heart Disease and Dilated Cardiomyopathy: Delineating at Single-Cell Level.Biomedicines · 2022Article
- Proteomic analysis identifies key differences in the cardiac interactomes of dystrophin and micro-dystrophin.Human molecular genetics · 2021Article
- Force-velocity and tension transient measurements from Drosophila jump muscle reveal the necessity of both weakly-bound cross-bridges and series elasticity in models of muscle contraction.Archives of biochemistry and biophysics · 2021Article
- Effect of a dianthin G analogue in the differentiation of rat bone marrow mesenchymal stem cells into cardiomyocytes.Molecular and cellular biochemistry · 2020Article
- Study of the Expression Transition of Cardiac Myosin Using Polarization-Dependent SHG Microscopy.Biophysical journal · 2020Article
- Role of MicroRNAs in Diagnosis, Prognosis, and Treatment of Acute Heart Failure: Ambassadors from Intracellular Zone.Galen medical journal · 2020Review
- A myosin-based mechanism for stretch activation and its possible role revealed by varying phosphate concentration in fast and slow mouse skeletal muscle fibers.American journal of physiology. Cell physiology · 2019Article
- Inflammatory Serine Proteases Play a Critical Role in the Early Pathogenesis of Diabetic Cardiomyopathy.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- Effect of fetal hypothyroidism on MyomiR network and its target gene expression profiles in heart of offspring rats.Molecular and cellular biochemistry · 2017Article
- The Drosophila indirect flight muscle myosin heavy chain isoform is insufficient to transform the jump muscle into a highly stretch-activated muscle type.American journal of physiology. Cell physiology · 2017Article
- Inhibition of Cardiac Hypertrophy Effects in D-Galactose-Induced Senescent Hearts byEvidence-based complementary and alternative medicine : eCAM · 2017Article
- L71F mutation in rat cardiac troponin T augments crossbridge recruitment and detachment dynamics against α-myosin heavy chain, but not against β-myosin heavy chain.Journal of muscle research and cell motility · 2016Article
- Comparison of elementary steps of the cross-bridge cycle in rat papillary muscle fibers expressing α- and β-myosin heavy chain with sinusoidal analysis.Journal of muscle research and cell motility · 2016Article
- Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats.Arquivos brasileiros de cardiologia · 2016Article
- Dilated Cardiomyopathy Mutation (R134W) in Mouse Cardiac Troponin T Induces Greater Contractile Deficits against α-Myosin Heavy Chain than against β-Myosin Heavy Chain.Frontiers in physiology · 2016Article
- Cardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent Activation.Frontiers in physiology · 2016Article
- Rat cardiac troponin T mutation (F72L)-mediated impact on thin filament cooperativity is divergently modulated by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
- The functional effect of dilated cardiomyopathy mutation (R144W) in mouse cardiac troponin T is differently affected by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The speed and force of myocardial contraction during systolic ejection is largely dependent on the intrinsic contractile properties of cardiac myocytes. As the myosin heavy chain (MHC) isoform of cardiac muscle is an important determinant of the contractile properties of individual myocytes, we studied the effects of altered MHC isoform expression in rat myocardium on the mechanical properties of skinned ventricular preparations. Skinned myocardium from thyroidectomized rats expressing only the beta MHC isoform displayed rates of force redevelopment that were about 2.5-fold slower than in myocardium from hyperthyroid rats expressing only the alpha MHC isoform, but the amount of force generated at a given level of Ca2+ activation was not different. Because recent studies suggest that the stretch activation response in myocardium has an important role in systolic function, we also examined the effect of MHC isoform expression on the stretch activation response by applying a rapid stretch (1% of muscle length) to an otherwise isometrically contracting muscle fibre. Sudden stretch of myocardium resulted in a concomitant increase in force that quickly decayed to a minimum and was followed by a delayed redevelopment of force (i.e. stretch activation) to levels greater than prestretch force. beta MHC expression dramatically slowed the overall rate of the stretch activation response compared to expression of alpha MHC isoform; specifically, the rate of force decay was approximately 2-fold slower and the rate of delayed force development was approximately 2.5-fold slower. In contrast, MHC isoform had no effect on the amplitude of the stretch activation response. Collectively, these data show that expression of beta MHC in myocardium dramatically slows rates of cross-bridge recruitment and detachment which would be expected to decrease power output and contribute to depressed systolic function in end-stage heart failure.
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Registered trials
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.