Vascular Extracellular Matrix and Arterial Mechanics

Abstract

An important factor in the transition from an open to a closed circulatory system was a change in vessel wall structure and composition that enabled the large arteries to store and release energy during the cardiac cycle. The component of the arterial wall in vertebrates that accounts for these properties is the elastic fiber network organized by medial smooth muscle. Beginning with the onset of pulsatile blood flow in the developing aorta, smooth muscle cells in the vessel wall produce a complex extracellular matrix (ECM) that will ultimately define the mechanical properties that are critical for proper function of the adult vascular system. This review discusses the structural ECM proteins in the vertebrate aortic wall and will explore how the choice of ECM components has changed through evolution as the cardiovascular system became more advanced and pulse pressure increased. By correlating vessel mechanics with physiological blood pressure across animal species and in mice with altered vessel compliance, we show that cardiac and vascular development are physiologically coupled, and we provide evidence for a universal elastic modulus that controls the parameters of ECM deposition in vessel wall development. We also discuss mechanical models that can be used to design better tissue-engineered vessels and to test the efficacy of clinical treatments.

Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

“…1,32 Our results are consistent with previous studies using the BCCA-L model, where we showed that BA caliber increased immediately after carotid ligation whereas WSS in the BA decreased sharply and returned to baseline within 4 to 5 weeks. 20 After this WSS normalization, there was no further increase in BA diameter.…”

Computational Simulation of the Adaptive Capacity of Vein Grafts in Response to Increased Pressure

“…This scenario may be consistent with cells trying to maintain local material stiffness while increasing structural stiffness to offset the increase in loading, which could be mechanically favorable [44].…”

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

“…The vessel wall of major arteries is composed of three connective tissue layers: an inner layer (tunica intima), a middle layer (tunica media), and an outer layer (tunica adventitia) (Wagenseil and Mecham 2009), each composed of different types of cells and ECM components (Fig. 4).…”

“…The internal elastic lamina separates the tunica intima from the tunica media, which is populated by vascular smooth muscle cells (VSMCs) and contains elastic fibers, complex structures that contain both elastin and fibrillin-containing microfibrils, collagen fibers, and proteoglycans (Wagenseil and Mecham 2009). Although the majority of VSMCs reside in the tunica media, some VSMCs or VSMC-like cells are also present in the tunica intima and/or can be recruited to the intima in response to vascular injury (Shanahan and Weissberg 1998;Owens et al 2004;Fukuda and Aikawa 2010;Iwata et al 2010).…”

“…The tunica intima, which is generally much thicker in human arteries compared with other mammals, does not contain elastic fibers. The outer layer or tunica adventitia is populated by adventitial fibroblasts, is rich in collagen, does not contain elastic fibers, and is separated by the tunica media by the external elastic lamina (reviewed in Wagenseil and Mecham 2009). Some studies have suggested that the adventitial layer contains progenitors that trans-differentiate into VSMCs (Sartore et al 2001;Hoofnagle et al 2004;Hu et al 2004;Passman et al 2008).…”