Mechanical strain memory in airway smooth muscle

2000 ◽  
Vol 278 (5) ◽  
pp. C895-C904 ◽  
Author(s):  
Wah-Lun Chan ◽  
Jeanette Silberstein ◽  
Chi-Ming Hai
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Mechanical Strain ◽  
Control Level ◽  
High Stress ◽  
Peak Stress ◽  
Airway Smooth Muscle Cells ◽  
Initial Length ◽  
Myosin Phosphorylation ◽  
Contraction And Relaxation

We investigated the effect of a single rapid stretch on poststretch force and myosin phosphorylation in bovine tracheal smooth muscle. When unstimulated muscle strips were stretched from suboptimal length to optimal length ( L o), poststretch steady-state force was not significantly different from that of unstretched control at L o. However, when carbachol-activated muscle strips were stretched from suboptimal length to L o, poststretch force and myosin phosphorylation were lower than control and significantly correlated with initial length. When poststretch muscle strips were allowed to relax for 1 h and then activated by K+ depolarization, the developed force remained significantly correlated with initial length. When the same strain was applied in 23 increments to minimize peak stress, poststretch force and myosin phosphorylation increased significantly, approaching the levels expected at L o. Furthermore, poststretch force development increased after each cycle of contraction and relaxation, approaching the control level after four cycles. These results suggest that activated airway smooth muscle cells can retain relatively precise memory of past strain when they are stretched rapidly with high stress.

Mechanisms of mechanical strain memory in airway smooth muscle

2005 ◽  
Vol 83 (10) ◽  
pp. 811-815 ◽  
Author(s):  
Hak Rim Kim ◽  
Chi-Ming Hai
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Mechanical Performance ◽  
Mechanical Strain ◽  
Muscle Cells ◽  
Cholinergic Receptor ◽  
Airway Smooth Muscle Cells ◽  
Deep Inspiration ◽  
Initial Length

We evaluated the hypothesis that mechanical deformation of airway smooth muscle induces structural remodeling of airway smooth muscle cells, thereby modulating mechanical performance in subsequent contractions. This hypothesis implied that past experience of mechanical deformation was retained (or "memorized") as structural changes in airway smooth muscle cells, which modulated the cell's subsequent contractile responses. We termed this phenomenon mechanical strain memory. Preshortening has been found to induce attenuation of both force and isotonic shortening velocity in cholinergic receptor-activated airway smooth muscle. Rapid stretching of cholinergic receptor-activated airway smooth muscle from an initial length to a final length resulted in post-stretch force and myosin light chain phosphorylation that correlated significantly with initial length. Thus post-stretch muscle strips appeared to retain memory of the initial length prior to rapid stretch (mechanical strain memory). Cytoskeletal recruitment of actin- and integrin- binding proteins and Erk 1/2 MAPK appeared to be important mechanisms of mechanical strain memory. Sinusoidal length oscillation led to force attenuation during oscillation and in subsequent contractions in intact airway smooth muscle, and p38 MAPK appeared to be an important mechanism. In contrast, application of local mechanical strain to cultured airway smooth muscle cells induced local actin polymerization and cytoskeletal stiffening. It is conceivable that deep inspiration-induced bronchoprotection may be a manifestation of mechanical strain memory such that mechan ical deformation from past breathing cycles modulated the mechanical performance of airway smooth muscle in subsequent cycles in a continuous and dynamic manner.Key words: airway, cytoskeleton, deep inspiration, mechanics, smooth muscle.

Mechanical strain increases velocity and extent of shortening in cultured airway smooth muscle cells

1999 ◽  
Vol 277 (2) ◽  
pp. L343-L348 ◽  
Author(s):  
Paul G. Smith ◽  
Chaity Roy ◽  
Jamie Dreger ◽  
Frank Brozovich
Keyword(s):  
Smooth Muscle ◽  
Mechanical Stress ◽  
Airway Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Mechanical Strain ◽  
Airway Smooth Muscle Cells ◽  
Maximal Velocity ◽  
Cell Contractility ◽  
Cell Shortening

Abnormal mechanical stress on lung tissue is associated with increased mass and contractility of airway smooth muscle (ASM). We have reported that cultured ASM cells subjected to cyclic strain exhibit increased myosin light chain kinase (MLCK) and stress filaments. Increased MLCK may increase contractile velocity, whereas increased stress filaments could impede cell shortening by increasing the cell’s internal load. To study strain-induced changes in cell contractility, the time course of shortening of individual cells exposed to 90 mM KCl was recorded. Length vs. time plots revealed significantly greater maximal velocity of shortening in strain cells than control (no strain). This correlated with an increase in MLCK and myosin light chain phosphorylation measured in strain cells in separate experiments. The extent of cell shortening tended to be greater in the strain cells so that increased impedance to shortening was not detected. Mechanical stress may therefore increase the contractility of ASM by increasing the content of MLCK.

Cyclic mechanical strain‐induced proliferation and migration of human airway smooth muscle cells: role of EMMPRIN and MMPs

2005 ◽  
Vol 19 (11) ◽  
pp. 1507-1509 ◽  
Author(s):  
Nadia A. Hasaneen ◽  
Stanley Zucker ◽  
Jian Cao ◽  
Christian Chiarelli ◽  
Reynold A. Panettieri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Mechanical Strain ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
And Migration ◽  
Proliferation And Migration

Localized mechanical stress induces time-dependent actin cytoskeletal remodeling and stiffening in cultured airway smooth muscle cells

2004 ◽  
Vol 287 (2) ◽  
pp. C440-C448 ◽  
Author(s):  
Linhong Deng ◽  
Nigel J. Fairbank ◽  
Ben Fabry ◽  
Paul G. Smith ◽  
Geoffrey N. Maksym
Keyword(s):  
Smooth Muscle ◽  
Mechanical Stress ◽  
Airway Smooth Muscle ◽  
Cell Function ◽  
Mechanical Strain ◽  
Cell Stiffness ◽  
Airway Smooth Muscle Cells ◽  
Airway Narrowing ◽  
Time Courses ◽  
Altered Cell

Mechanical stress (MS) causes cytoskeletal (CSK) and phenotypic changes in cells. Such changes in airway smooth muscle (ASM) cells might contribute to the pathophysiology of asthma. We have shown that periodic mechanical strain applied to cultured ASM cells alters the structure and expression of CSK proteins and increases cell stiffness and contractility (Smith PG, Moreno R, and Ikebe M. Am J Physiol Lung Cell Mol Physiol 272: L20–L27, 1997; and Smith PG, Deng L, Fredberg JJ, and Maksym GN. Am J Physiol Lung Cell Mol Physiol 285: L456–L463, 2003). However, the mechanically induced CSK changes, altered cell function, and their time courses are not well understood. Here we applied MS to the CSK by magnetically oscillating ferrimagnetic beads bound to the CSK. We quantified CSK remodeling by measuring actin accumulation at the sites of applied MS using fluorescence microscopy. We also measured CSK stiffness using optical magnetic twisting cytometry. We found that, during MS of up to 120 min, the percentage of beads associated with actin structures increased with time. At 60 min, 68.1 ± 1.6% of the beads were associated with actin structures compared with only 6.7 ± 2.8% before MS and 38.4 ± 5.5% in time-matched controls ( P < 0.05). Similarly, CSK stiffness increased more than twofold in response to the MS compared with time-matched controls. These changes were more pronounced than observed with contractile stimulation by 80 mM KCl or 10−4 M acetylcholine. Together, these findings imply that MS is a potent stimulus to enhance stiffness and contractility of ASM cells through CSK remodeling, which may have important implications in airway narrowing and dilation in asthma.

Mechanical strain increases contractile enzyme activity in cultured airway smooth muscle cells

1995 ◽  
Vol 268 (6) ◽  
pp. L999-L1005 ◽  
Author(s):  
P. G. Smith ◽  
T. Tokui ◽  
M. Ikebe
Keyword(s):  
Smooth Muscle ◽  
Atpase Activity ◽  
Airway Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Mechanical Strain ◽  
Physical Stress ◽  
Airway Smooth Muscle Cells ◽  
Myosin Light Chain Phosphatase ◽  
Actomyosin Atpase

Smooth muscle hypertrophy is often found in tissue subjected to abnormal physical stress. To determine if physical stress (strain) per se could increase the contractile potential of airway smooth muscle (ASM), we compared cultured ASM cells subjected to strain to control cells (no strain) for rates of 1) myosin light chain kinase (MLCK)-mediated myosin light chain (LC20) phosphorylation, 2) actin-activated myosin ATPase, and 3) myosin light chain phosphatase-mediated myosin dephosphorylation. Lysates from strained cells showed increases in both LC20 phosphorylation activity and actomyosin ATPase activity but decreased rates of phosphatase-dependent myosin dephosphorylation. The increased LC20 phosphorylation activity and ATPase activity of the strained cells were accompanied by increases in cellular content of MLCK and myosin, respectively, compared with control. Because the cultured ASM cells exposed to strain expressed higher MLCK activity and actomyosin ATPase activity but lower myosin light chain phosphatase activity, these data suggest that physical stress in part determines ASM potential for contractile state.

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