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Somali Chaterji. 1 Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, Texas.
Peter Kim. 2 Department of Bioengineering, University of Washington, Seattle, Washington.
Seung H. Choe. 1 Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, Texas.
Jonathan H. Tsui. 2 Department of Bioengineering, University of Washington, Seattle, Washington.
Christoffer H. Lam. 1 Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, Texas.
Derek S. Ho. 1 Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, Texas.
Aaron B. Baker. 1 Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, Texas.
Deok-Ho Kim. 2 Department of Bioengineering, University of Washington, Seattle, Washington. 3 Center for Cardiovascular Biology, University of Washington, Seattle, Washington. 4 Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington.
Address correspondence to: Deok-Ho Kim, PhD, Department of Bioengineering, University of Washington, Box 355061, Seattle, WA 98195, E-mail: [email protected]
Aaron B. Baker, PhD, Department of Biomedical Engineering, Cockrell School of Engineering, The University of Texas at Austin, 1 University Station, BME 5.202D, MC C0800, Austin, TX 78712, E-mail: [email protected]
Introduction
Vascular smooth muscle cells (vSMCs) regulate the vasomotor tone of blood vessels by virtue of their contractile function. However, given the need for long-term adaptation through structural remodeling in pregnancy, exercise, or vascular injury, vSMCs retain the ability to undergo modulation in their phenotypic continuum. This continuum ranges from a mature contractile state to a proliferative, secretory state; these states differ in the expression of vSMC-restricted contractile protein genes, which strikingly contain the conserved CArG box DNA sequences within their promoters.1-3 vSMC differentiation is modulated by a complex array of microenvironmental cues, which include the biochemical milieu of the cells and the architecture and stiffness of the extracellular matrix (ECM). It is known that ECM proteins such as elastin and collagen, comprising the bulk of the ECM of the tunica media, present a nanoscale architecture,4 that can potentially control the polarization of vSMCs in the artery. While there is some debate on the specific orientation of vSMCs in the arterial wall,5 it is clear...