Abstract
Tenascins are a family of multifunctional extracellular matrix (ECM) glycoproteins with time- and tissue specific expression patterns during development, tissue homeostasis, and diseases. There are four family members (tenascin-C, -R, -X, -W) in vertebrates. Among them, tenascin-X (TNX) and tenascin-C (TNC) play important roles in human pathologies. TNX is expressed widely in loose connective tissues. TNX contributes to the stability and maintenance of the collagen network, and its absence causes classical-like Ehlers-Danlos syndrome (clEDS), a heritable connective tissue disorder. In contrast, TNC is specifically and transiently expressed upon pathological conditions such as inflammation, fibrosis, and cancer. There is growing evidence that TNC is involved in inflammatory processes with proinflammatory or anti-inflammatory activity in a context-dependent manner. In this review, we summarize the roles of these two tenascins, TNX and TNC, in cardiovascular and inflammatory diseases and in clEDS, and we discuss the functional consequences of the expression of these tenascins for tissue homeostasis.
Highlights
An important component of the extracellular environment is the extracellular matrix (ECM), which is comprised of glycoproteins, proteoglycans, and fibrillar proteins
The tenascin family members have a common structure with heptad repeats, epidermal growth factor (EGF)-like repeats, fibronectin type III (FNIII)-like repeats, and a fibrinogen (FBG)-related domain
We have shown that TNX interacts with vascular endothelial growth factor B (VEGF-B) and stimulates endothelial cell proliferation via simultaneous binding to VEGF receptor 1 (VEGFR-1) and VEGF-B [52]
Summary
An important component of the extracellular environment is the extracellular matrix (ECM), which is comprised of glycoproteins, proteoglycans, and fibrillar proteins. In agreement with the tumor suppressor role of TNX in cancer progression, TNX-deficient mice with grafted melanoma cells exhibited promotion of tumor invasion and metastasis because of increased activities of matrix metalloproteinases (MMPs) [37, 38]. The results of a number of studies on abnormalities in mice with targeted deletion in Tnxb [40] and in clEDS patients [26, 41] have suggested structural roles of TNX in tissue integrity [7, 42].
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