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Am J Physiol Cell Physiol (August 24, 2005). doi:10.1152/ajpcell.00060.2005
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Submitted on February 11, 2005
Accepted on July 9, 2005

The rat airway smooth muscle cell during actin modulation: rheology and glassy dynamics

Rachel E Laudadio1, Emil J Millet1, Ben Fabry2, Steven S An1, James P Butler1, and Jeffrey J Fredberg1*

1 Environmental Health, Harvard School of Public Health, Boston, MA, USA
2 Physics, Erlangen University, Erlangen, Germany

* To whom correspondence should be addressed. E-mail: jfredber{at}hsph.harvard.edu.

Although changes of cytoskeletal (CSK) stiffness and friction can be induced by diverse interventions, all mechanical changes reported to date can be scaled onto master relationships that appear to be universal. To assess the limits of applicability of those master relationships, here we focused on actin and employed a panel of actinmanipulating drugs that is much wider than any used previously. As a model system we focused on the cultured rat airway smooth muscle (ASM) cell. Cells were treated with agents that directly modulate the polymerization (jasplakinolide, cytochalasin D, latrunculin A), branching (genistein), and cross-linking (phallacidin, phalloidin oleate) of the actin lattice. Contractile (5-HT) and relaxing (db cAMP) agonists and a myosin inhibitor (ML-7) were also tested for comparison since these agents may change the structure of actin indirectly. Using optical magnetic twisting cytometry, elastic and frictional moduli were measured before and after treatment with each agent. Stiffness increased with frequency as a weak power law, and changes of friction paralleled those of stiffness until they approached a Newtonian viscous limit. Despite large differences in the mechanism of action among the interventions, all data collapsed onto master curves that depended upon a single parameter. In the context of soft glassy systems, that parameter would correspond to an effective temperature of the cytoskeletal matrix and reflect the effects of extreme molecular crowding and associated molecular trapping. These master relationships demonstrate that when the mechanical properties of the cell change, they are constrained to do so along a special trajectory. Since mechanical characteristics of the cell shadow underlying molecular events, these results imply special constraints upon the protein-protein interactions that dominate CSK mechanical properties.




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