| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115; 2Department of Pharmacology, University of Nevada, Reno, Nevada 89557; 3Pulmonary and Critical Care Division, Tufts-New England Medical Center, Boston, Massachusetts 02111; and 4Institute of Biochemistry, Hannover Medical School, 30625 Hannover, Germany
Submitted 17 October 2003 ; accepted in final form 7 January 2004
Remodeling of the airway smooth muscle (ASM) cell has been proposed to play an important role in airway hyperresponsiveness. Using a functional assay, we have assessed remodeling of the cultured rat ASM cell and the role of heat shock protein (HSP) 27 in that process. To probe remodeling dynamics, we measured spontaneous motions of an individual Arg-Gly-Asp-coated microbead that was anchored to the cytoskeleton. We reasoned that the bead could not move unless the microstructure to which it is attached rearranged; if so, then its mean square displacement (MSD) would report ongoing internal reorganizations over time. Each bead displayed a random, superdiffusive motion; MSD increased with time as 
t1.7, whereas an exponent of unity would be expected for a simple passive diffusion. Increasing concentrations of cytochalasin-D or latrunculin-A caused marked increases in the MSD, whereas colchicine did not. Treatments with PDGF or IL-1
, but not transforming growth factor-, caused decreases in the MSD, the extent of which rank-ordered with the relative potency of these agents in eliciting the phosphorylation of HSP27. The chemical stressors anisomycin and arsenite each increased the levels of HSP27 phosphorylation and, at the same time, decreased bead motions. In particular, arsenite prevented and even reversed the effects of cytochalasin-D on bead motions. Finally, ASM cells overexpressing phospho-mimicking human HSP27, but not wild-type or phosphorylation-deficient HSP27, exhibited decreases in bead motions that were comparable to the arsenite response. Taken together, these results show that phosphorylated HSP27 favors reduced bead motions that are probably due to stabilization of the actin cytoskeleton.
cytoskeleton; plasticity; actin dynamics; diffusion; superdiffusion
This article has been cited by other articles:
|
|
 |
|
  E. H. Zhou, X. Trepat, C. Y. Park, G. Lenormand, M. N. Oliver, S. M. Mijailovich, C. Hardin, D. A. Weitz, J. P. Butler, and J. J. Fredberg Universal behavior of the osmotically compressed cell and its analogy to the colloidal glass transition PNAS, June 30, 2009; 106(26): 10632 - 10637. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Chaudhuri and P. G. Smith Cyclic Strain-Induced HSP27 Phosphorylation Modulates Actin Filaments in Airway Smooth Muscle Cells Am. J. Respir. Cell Mol. Biol., September 1, 2008; 39(3): 270 - 278. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Gunst and W. Zhang Actin cytoskeletal dynamics in smooth muscle: a new paradigm for the regulation of smooth muscle contraction Am J Physiol Cell Physiol, September 1, 2008; 295(3): C576 - C587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Liao, Z. Liu, J. Bao, Z. Zhao, J. Hu, X. Feng, R. Feng, Q. Lu, Z. Mei, Y. Liu, et al. A proteomic study of the aortic media in human thoracic aortic dissection: Implication for oxidative stress J. Thorac. Cardiovasc. Surg., July 1, 2008; 136(1): 65 - 72. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Srinivasan, S. Forman, R. A. Quinlan, J. Ohanian, and V. Ohanian Regulation of contractility by Hsp27 and Hic-5 in rat mesenteric small arteries Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H961 - H969. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. An, T. R. Bai, J. H. T. Bates, J. L. Black, R. H. Brown, V. Brusasco, P. Chitano, L. Deng, M. Dowell, D. H. Eidelman, et al. Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma Eur. Respir. J., May 1, 2007; 29(5): 834 - 860. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. R. Jog, V. R. Jala, R. A. Ward, M. J. Rane, B. Haribabu, and K. R. McLeish Heat Shock Protein 27 Regulates Neutrophil Chemotaxis and Exocytosis through Two Independent Mechanisms J. Immunol., February 15, 2007; 178(4): 2421 - 2428. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. J. M. Brundel, A. Shiroshita-Takeshita, X. Qi, Y.-H. Yeh, D. Chartier, I. C. van Gelder, R. H. Henning, H. H. Kampinga, and S. Nattel Induction of Heat Shock Response Protects the Heart Against Atrial Fibrillation Circ. Res., December 8, 2006; 99(12): 1394 - 1402. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Lu, E. O. Harrington, H. Jackson, N. Morin, C. Shannon, and S. Rounds Transforming growth factor-beta1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation J Appl Physiol, August 1, 2006; 101(2): 375 - 384. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. S. An, C. M. Pennella, A. Gonnabathula, J. Chen, N. Wang, M. Gaestel, P. M. Hassoun, J. J. Fredberg, and U. S. Kayyali Hypoxia alters biophysical properties of endothelial cells via p38 MAPK- and Rho kinase-dependent pathways Am J Physiol Cell Physiol, September 1, 2005; 289(3): C521 - C530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.G. Stewart Emigration and immigration of mesenchymal cells: a multicultural airway wall Eur. Respir. J., October 1, 2004; 24(4): 515 - 517. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
