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Abstract Stiffening of the extracellular matrix (ECM) occurs after vascular injury and contributes to the injury-associated proliferation of vascular smooth muscle cells (SMCs). ECM stiffness also activates Rac-GTP, and SMC Rac1 deletion strongly reduces the proliferative response to injury in vivo. However, ECM stiffening and Rac can affect SMC differentiation, which, in itself, can influence ECM stiffness and proliferation.
The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms/processes that control differentiation of vascular smooth muscle cells (SMC) during normal development and maturation of the vasculature, as well as how these mechanisms/processes are altered in vascular injury or disease.
ECM-coated polyacrylamide hydrogels have been used extensively to study how cells sense and respond to the physical characteristics of their microenvironments because their tunable mechanical properties can mimic the physiological and pathological elasticity of tissues38,39. To investigate role of CD44 in stiffness-dependent motility, we generated FN-coated polyacrylamide hydrogels of elastic moduli ranging from 2–4 kPa (hereafter called “soft”) to 18–20 kPa (hereafter called “stiff”).
In vivo, cells respond to a host of physical cues ranging from substrate stiffness to the organization of micro- and nanoscale fibrous networks. We show that macroscale substrates with radii of curvature from tens to hundreds of micrometers influence cell alignment. In a model system of fibroblasts, isolated cells aligned strongly in the axial direction on cylinders with radii similar to the cell length and more weakly on cylinders of much larger radius.
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