HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gerthoffer, W. T. Search for Related Content PubMed PubMed Citation Articles by Gerthoffer, W. T.

Migration of Airway Smooth Muscle Cells

Department of Pharmacology, University of Nevada School of Medicine, Reno, Nevada

Correspondence and requests for reprints should be addressed to William T. Gerthoffer, Ph.D., Department of Biochemistry, University of South Alabama, Mobile, AL 36688. E-mail: wgerthoffer{at}usouthal.edu

ABSTRACT

Migration of smooth muscle cells is a process fundamental to development of hollow organs, including blood vessels and the airways. Migration is also thought to be part of the response to tissue injury. It has also been suggested to contribute to airways remodeling triggered by chronic inflammation. In both nonmuscle and smooth muscle cells numerous external signaling molecules and internal signal transduction pathways contribute to cell migration. The review includes evidence for the functional significance of airway smooth muscle migration, a summary of promigratory and antimigratory agents, and summaries of important signaling pathways mediating migration. Important signaling pathways and effector proteins described include small G proteins, phosphatidylinositol 3-kinases (PI3-K), Rho activated protein kinase (ROCK), p21-activated protein kinases (PAK), Src family tyrosine kinases, and mitogen-activated protein kinases (MAPK). These signaling modules control multiple critical effector proteins including actin nucleating, capping and severing proteins, myosin motors, and proteins that remodel microtubules. Actin filament remodeling, focal contact remodeling and propulsive force of molecular motors are all coordinated to move cells along gradients of chemical cues, matrix adhesiveness, or matrix stiffness. Airway smooth muscle cell migration can be modulated in vitro by drugs commonly used in pulmonary medicine including β-adrenergic agonists and corticosteroids. Future studies of airway smooth muscle cell migration may uncover novel targets for drugs aimed at modifying airway remodeling.

Key Words: asthma • actin • cytokines • cytoskeleton • signal transduction

This article has been cited by other articles:

				H. H. Wang, A. Nakamura, A. Matsumoto, S. Yoshiyama, X. Qin, L.-H. Ye, C. Xie, Y. Zhang, Y. Gao, R. Ishikawa, et al. Nonkinase activity of MLCK in elongated filopodia formation and chemotaxis of vascular smooth muscle cells toward sphingosylphosphorylcholine Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1683 - H1693. [Abstract] [Full Text] [PDF]

				M.-C. Maa, M. Y. Chang, Y.-J. Chen, C.-H. Lin, C. J. Yu, Y. L. Yang, J. Li, P.-R. Chen, C.-H. Tang, H.-Y. Lei, et al. Requirement of Inducible Nitric-oxide Synthase in Lipopolysaccharide-mediated Src Induction and Macrophage Migration J. Biol. Chem., November 14, 2008; 283(46): 31408 - 31416. [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]