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(Circulation Research. 2007;101:651.)
© 2007 American Heart Association, Inc.

Editorials

7ß1 Integrin

Putting the Brakes on Smooth Muscle Cell Proliferation

Emily Wilson

From the Department of Systems Biology and Translational Medicine, Texas A&M Health Science Center, College of Medicine, College Station.

Correspondence to Emily Wilson, PhD, Associate Professor, Department of Systems Biology and Translational Medicine, Texas A&M Health Science Center, College of Medicine, College Station TX 77843-1114. E-mail emilyw@tamu.edu

See related article, pages 672–681

Key Words: phenotypic modulation • signal transduction • vascular injury • adhesion molecules

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

Modulation of smooth muscle cell (SMC) differentiation status is an important aspect of vascular development, normal differentiation and function, and pathogenesis of various diseases including atherosclerosis, hypertension, and aneurysms. SMCs are not terminally differentiated and possess the ability to change phenotype in response to local environmental cues. Thus, changes in the local environment contribute to the switching of SMCs from the normal contractile phenotype to more proliferative, synthetic phenotypes that are present in these diseases.^1,2 The molecular mechanisms regulating smooth muscle phenotypic modulation are only now beginning to be understood, and how input from the extracellular matrix impacts these changes is still an area of ongoing research. In the current issue of Circulation Research, Welser et al³ investigate the contribution of the laminin binding integrin 7ß1 to phenotypic modulation of SMCs.

Adhesion to specific extracellular matrix (ECM) proteins is known to modulate the phenotypic status of SMCs in culture, and altered expression of ECM proteins in vivo correlate with changes in the status of SMCs and with vascular pathologies such as hypertension and atherosclerosis.^4,5 Thyberg⁶ reviewed the contributions of various ECM molecules to smooth muscle status and reported that SMCs grown on fibronectin (and other transitional matrices) showed increased proliferation, whereas cells on laminin and other basement membrane proteins proliferated slower and expressed larger quantities of smooth muscle specific contractile proteins. In addition, we^7,8and others⁹ showed that the type of ECM influences the response of SMC to mechanical stimulation. The differences between these SMCs are thought to arise . . . [Full Text of this Article]

Related Article:

Loss of the 7 Integrin Promotes Extracellular Signal-Regulated Kinase Activation and Altered Vascular Remodeling

Jennifer V. Welser, Naomi Lange, Cherie A. Singer, Margaret Elorza, Paul Scowen, Kathleen D. Keef, William T. Gerthoffer, and Dean J. Burkin
Circ. Res. 2007 101: 672-681. [Abstract] [Full Text] [PDF]