This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jones, P. L. Search for Related Content PubMed PubMed Citation Articles by Jones, P. L. Related Collections Related Article

(Circulation Research. 2007;100:757.)
© 2007 American Heart Association, Inc.

Editorials

Move On!

Smooth Muscle Cell Motility Paired Down

Peter Lloyd Jones

From the Institute for Medicine and Engineering, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia.

Correspondence to Peter Lloyd Jones, Associate Professor, Pathology and Laboratory Medicine, Institute for Medicine and Engineering, University of Pennsylvania, 1010 Vagelos Research Laboratories, 3340 Smith Walk, Philadelphia, PA 19104-6383. E-mail jonespl@mail.med.upenn.edu

See related article, pages 817–825

Key Words: motility • homeobox genes • Prx1 • matrix • smooth muscle • tenascin-C

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
A cardinal feature of the response to injury within the muscularized, adult blood vessel wall is the transformation of an highly organized, isometric, cytoskeletal archetype, housed within vascular smooth muscle cells (SMCs), to one that supports cell migration, the function of which is to elicit repair.¹ Such reorganization of the SMC cytoskeleton permits cells to move from the comfort of their controlled environment, which includes the surrounding extracellular matrix (ECM) and their neighboring cells, to the site of injury. Cytoskeletal remodeling also initiates other functions required for the injury-repair response, including SMC proliferation, and the creation of a provisional ECM that supports cell motility, growth and survival.^2,3 For the most part, these and many other repair-related processes, including the recruitment and differentiation of inflammatory and stem cells to sites of injury,^4,5 are coordinated through changes in cell-cell and cell–matrix adhesion, which collectively act with numerous other intrinsic and extrinsic factors, to stimulate or repress programs of signal transduction and gene expression. Sometimes, however, overexuberant responses to injury lead to hyper-repair of blood vessels, leaving them occluded and functionless.^1,6 Thus, identifying molecules and pathways that control cytoskeletal homeostasis and remodeling represents a critical step in comprehending how blood vessels develop, and how SMCs contained therein adapt to injury in the fetal-, neo-, and postnatal periods.

With respect to the general cellular mechanisms leading to increased SMC motility, reorganization of the cytoskeleton relies on the recruitment of multiple signaling and adaptor proteins to focal or fibrillar adhesion sites that reiteratively form, deconstruct . . . [Full Text of this Article]

Related Article:

Angiotensin II, Focal Adhesion Kinase, and PRX1 Enhance Smooth Muscle Expression of Lipoma Preferred Partner and its Newly Identified Binding Partner Palladin to Promote Cell Migration

Li Jin, Michael J. Kern, Carol A. Otey, Brian R. Wamhoff, and Avril V. Somlyo
Circ. Res. 2007 100: 817-825. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				L. Jin, T. Yoshida, R. Ho, G. K. Owens, and A. V. Somlyo The Actin-associated Protein Palladin Is Required for Development of Normal Contractile Properties of Smooth Muscle Cells Derived from Embryoid Bodies J. Biol. Chem., January 23, 2009; 284(4): 2121 - 2130. [Abstract] [Full Text] [PDF]