Applicability of the sliding filament/crossbridge paradigm to smooth muscle

Gunst, Susan J.

doi:10.1007/3-540-64753-8_2

Cited by 12 publications

(12 citation statements)

References 226 publications

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“…This could enable the smooth muscle cell to adapt the arrangement of its contractile apparatus to externally imposed changes in the shape of the cell. In tracheal smooth muscle, contractile activation at different lengths results in persistent differences in stiffness that suggest differences in cell structure (Gunst et al 1995; Gunst & Wu, 1996; Gunst, 1999).…”

Section: Discussionmentioning

confidence: 99%

Actin polymerization stimulated by contractile activation regulates force development in canine tracheal smooth muscle

Mehta

Gunst

1999

The Journal of Physiology

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224

295

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Section: Discussionmentioning

confidence: 99%

Actin polymerization stimulated by contractile activation regulates force development in canine tracheal smooth muscle

Mehta

Gunst

1999

The Journal of Physiology

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224

295

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“…Dynamic changes in cytoskeletal organization have been proposed as a mechanism by which airway smooth muscle cells may modulate their structure and contractility to accommodate to changes in their external environment (25,(31)(32)(33). Actin polymerization and remodeling form the basis for regulating the shape and stiffness of many cell types, and it is therefore plausible that smooth muscle cells might also depend on similar processes to adapt their shape and stiffness to external conditions.…”

Section: Cytoskeletal Dynamics In Airway Smooth Muscle Cells During Cmentioning

confidence: 99%

Interactions of Airway Smooth Muscle Cells with Their Tissue Matrix: Implications for Contraction

Zhang¹,

Gunst²

2008

Proceedings of the American Thoracic Society

109

108

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The ability of airway smooth muscle to alter its stiffness and contractility in response to mechanical oscillation and stretch is critically important for the regulation of normal airway responsiveness during breathing. The properties of mechanical adaptation in airway smooth muscle are proposed to result from dynamic cytoskeletal processes outside of the actomyosin interaction. The actomyosin interaction and crossbridge cycling are viewed as components of a complex and integrated array of cytoskeletal events that occur during cell contraction. These events are orchestrated by macromolecular protein complexes that associate with the cytoplasmic domains of integrin proteins at the adhesion junctions between muscle cells and the extracellular matrix. According to this paradigm, these concerted cytoskeletal events are essential components of the process of active tension generation in airway smooth muscle, and also serve to adapt the shape and stiffness of the smooth muscle cell to its environment. Contractile stimuli initiate actin polymerization within the submembranous cortex of the airway smooth muscle cell that may serve to determine the cells shape and strengthen the membrane. The recruitment of structural proteins such as alpha-actinin to adhesion junctions fortifies the strength of the connections between membrane adhesion junctions and actin filaments. These processes create a strong and rigid cytoskeletal framework for the transmission of force generated by the interaction of myosin and actin filaments. This model for the regulation of airway smooth muscle function can provide novel perspectives to explain the normal physiologic behavior of the airways and pathophysiologic properties of the airways in asthma.

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“…Using other types of experiments, our colleague, Dr. Susan Gunst, has proposed that the thin filaments are also labile, and this lability may enhance plasticity (reviewed by Gunst 1999). Using other types of experiments, our colleague, Dr. Susan Gunst, has proposed that the thin filaments are also labile, and this lability may enhance plasticity (reviewed by Gunst 1999).…”

Section: Relationship To Other Workmentioning

confidence: 99%

Plasticity in airway smooth muscle: an update

Ford¹

2005

Can. J. Physiol. Pharmacol.

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At a similar meeting 10 years ago, we proposed (i) that the long functional range of some smooth muscles is accommodated by plastic alterations that place more myofilaments in series at longer lengths, (ii) that this plasticity is facilitated by myosin filament evanescence, with filaments dissociating partially during relaxation and reforming upon activation, and (iii) that filament lengthening during the rise of activation would cause velocity to fall. Since that meeting, we have accumulated a substantial body of evidence to support these proposals, as follows: (i) muscles develop nearly the same force when adapted to a range of lengths that can vary by 3-fold; (ii) other physiological parameters including shortening velocity, maximum power, compliance, ATPase rate, and thick-filament mass increase by about 2/3 for a doubling of muscle length; (iii) thick-filament density increases substantially during the rise of activation; and (iv) velocity falls as force rises during the rise of tetanic force, and when correction is made for differences in activation, velocity and force vary exactly in inverse proportion. This review explains the rationale for the different experimental measurements and their interpretation.

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Applicability of the sliding filament/crossbridge paradigm to smooth muscle

Cited by 12 publications

References 226 publications

Actin polymerization stimulated by contractile activation regulates force development in canine tracheal smooth muscle

Actin polymerization stimulated by contractile activation regulates force development in canine tracheal smooth muscle

Interactions of Airway Smooth Muscle Cells with Their Tissue Matrix: Implications for Contraction

Plasticity in airway smooth muscle: an update

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