Blood vessels constantly subjected to mechanical stress have well-developed elastic fiber-rich frameworks, which contribute to the elasticity and distensibility of the vascular wall. Destruction of the fibrous structure due to genetic predisposition as well as acquired disorders such as Kawasaki disease often induces irreversible dilation of blood vessels, e.g., aneurysm formation. In addition to their structural role, extracellular matrix molecules also provide important biological signaling, which influences various cellular functions. Among them, increased attention has been focused on matricellular proteins, a group of nonstructural extracellular matrix (ECM) proteins highly upregulated in active tissue remodeling, serving as biological mediators by interacting directly with cells or regulating the activities of growth factors, cytokines, proteases, and other ECM molecules. Tenascin-C (TNC) is a typical matricellular protein expressed during embryonic development and tissue repair/regeneration in a spatiotemporally restricted manner. Various growth factors, pro-inflammatory cytokines, and mechanical stress upregulate its expression. TNC controls cell adhesion, migration, differentiation, and synthesis of ECM molecules. Our recent results suggest that TNC may not only play a significant role in the recruitment of smooth muscle/mural cells during vascular development, but also regulate the inflammatory response during pathological remodeling. TNC may be a key molecule during vascular development, adaptation, and pathological tissue remodeling.
Copyright 2016, The Author(s).