doi: 10.1161/01.RES.0000263446.33849.ed
© 2007 American Heart Association, Inc.
Editorials |
Move On!
Smooth Muscle Cell Motility Paired Down
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. |
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Introduction |
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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
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