ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Force maintenance and myosin filament assembly regulated by Rho-kinase in airway smooth muscle.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Circulating microRNAs associated with bronchodilator response in childhood asthma.BMC pulmonary medicine · 2024Article
- Review
- Review
- Filament evanescence of myosin II and smooth muscle function.The Journal of general physiology · 2021Review
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Inhibition of Rho-kinase improves response to deep inspiration in ovalbumin-sensitized guinea pigs.Iranian journal of basic medical sciences · 2020Article
- Tissue traction microscopy to quantify muscle contraction within precision-cut lung slices.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Airway smooth muscle tone increases actin filamentogenesis and contractile capacity.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility.Frontiers in physiology · 2020Review
- Molecular Mechanisms for the Mechanical Modulation of Airway Responsiveness.Journal of engineering and science in medical diagnostics and therapy · 2019Article
- Mechanopharmacology and Synergistic Relaxation of Airway Smooth Muscle.Journal of engineering and science in medical diagnostics and therapy · 2019Article
- The Aftermath of Bronchoconstriction.Journal of engineering and science in medical diagnostics and therapy · 2019Review
- Epithelial vertex models with active biochemical regulation of contractility can explain organized collective cell motility.APL bioengineering · 2018Article
- Rho kinase collaborates with p21-activated kinase to regulate actin polymerization and contraction in airway smooth muscle.The Journal of physiology · 2018Article
- Transient stretch induces cytoskeletal fluidization through the severing action of cofilin.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Effect of Rho-kinase inhibition on complexity of breathing pattern in a guinea pig model of asthma.PloS one · 2017Article
- Apical Sarcomere-like Actomyosin Contracts Nonmuscle Drosophila Epithelial Cells.Developmental cell · 2016Article
- Inhibition of PI3K promotes dilation of human small airways in a rho kinase-dependent manner.British journal of pharmacology · 2016Article
- Static and dynamic stress heterogeneity in a multiscale model of the asthmatic airway wall.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Cryopreserved Human Precision-Cut Lung Slices as a Bioassay for Live Tissue Banking. A Viability Study of Bronchodilation with Bitter-Taste Receptor Agonists.American journal of respiratory cell and molecular biology · 2016Article
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Authors and funding
14 authors.
Funding
Abstract
Smooth muscle contraction can be divided into two phases: the initial contraction determines the amount of developed force and the second phase determines how well the force is maintained. The initial phase is primarily due to activation of actomyosin interaction and is relatively well understood, whereas the second phase remains poorly understood. Force maintenance in the sustained phase can be disrupted by strains applied to the muscle; the strain causes actomyosin cross-bridges to detach and also the cytoskeletal structure to disassemble in a process known as fluidization, for which the underlying mechanism is largely unknown. In the present study we investigated the ability of airway smooth muscle to maintain force after the initial phase of contraction. Specifically, we examined the roles of Rho-kinase and protein kinase C (PKC) in force maintenance. We found that for the same degree of initial force inhibition, Rho-kinase substantially reduced the muscle's ability to sustain force under static conditions, whereas inhibition of PKC had a minimal effect on sustaining force. Under oscillatory strain, Rho-kinase inhibition caused further decline in force, but again, PKC inhibition had a minimal effect. We also found that Rho-kinase inhibition led to a decrease in the myosin filament mass in the muscle cells, suggesting that one of the functions of Rho-kinase is to stabilize myosin filaments. The results also suggest that dissolution of myosin filaments may be one of the mechanisms underlying the phenomenon of fluidization. These findings can shed light on the mechanism underlying deep inspiration induced bronchodilation.
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