Journal of Applied Physiology AJP: Heart and Circulatory Physiology
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J Appl Physiol (December 14, 2001). doi:10.1152/japplphysiol.00782.2001
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Articles in PresS, published online ahead of print December 14, 2001
J Appl Physiol, 10.1152/jap.00782.2001
Submitted on July 25, 2001
Accepted on December 3, 2001

The effect of the cytoskeletal prestress on the mechanical impedance of cultured airway smooth muscle cells

Dimitrije Stamenovic1*, Zhuangli Liang1, Jianxin Chen2, and Ning Wang2

1 Department of Biomedical Engineering, Boston University, Boston, Massachusetts, USA
2 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA

* To whom correspondence should be addressed. E-mail: dimitrij{at}engc.bu.edu.

We investigated the effect of the cytoskeletal prestress (P)on the elastic and frictional properties of cultured human airway smooth muscle (HASM) cells during oscillatory loading; P is preexisting tensile stress in the actin cytoskeleton generated by the cell contractile apparatus. We oscillated (0.1 Hz, 6 Pa peak-to-peak) small ferromagnetic beads bound to integrin receptors and computed the storage (elastic) modulus (G') and the loss (frictional) modulus (G") from the applied torque and the corresponding bead rotation. All measurements were done at baseline and after cells were treated with either graded doses of histamine (0.1, 1, 10 µM) or isoproterenol (0.01, 0.1, 1, 10 µM). Values for P for these concentrations were taken from a previous study (Am. J. Physiol. Cell Physiol., in press). It was found that G' and G", as well as P, increased/decreased with increasing doses of histamine/isoproterenol. Both G' and G" exhibited linear dependences on P: G'(Pa) = 0.20P + 82 and G"(Pa) = 0.05P + 32. The dependence of G' on P is consistent with our previous findings and with the behavior of stress-supported structures. The dependence of G" on P is a novel finding. It could be attributed to a variety of mechanisms. Some of those mechanisms are discussed in detail. We concluded that in addition to the central mechanisms by which stress-supported structures develop mechanical stresses, other mechanisms might need to be invoked to fully explain the observed dependence of the cell mechanical properties on the state of cell contractility.




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