Anti-adhesive matrix molecules

While a lack of cell adhesion will not promote cell survival or proliferation, there are several physiological processes that depend upon cell detachment from the ECM. Examples of this necessary de-adhesion can be found in normal development and tissue homeostasis, as anti-adhesive molecules cause different levels of de-adhesion ranging from complete cell detachment to the localized detachment required for cell migration. Investigation of these anti-adhesive molecules is important, as their use in biomaterials may provide a means to generate matrices that are conducive to cell migration by mimicking the adhesive/anti-adhesive nature of the native ECM. 

Anti-adhesive molecules affect cell adhesion by changing the arrangement of cytoskeletal proteins and by altering signaling cascades. Specifically, tenascin-C, TSP-1, and SPARC all downregulate the actin stress fiber system and disrupt focal adhesions when added in solution to spread cells (Murphy-Ullrich, 2001 Orend and Chiquet-Ehrismann, 2000). Reorganization of the actin cytoskeleton is a major pathway by which 

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Chiquet-Ehrismann, R. (1991) Anti-adhesive molecules of the extracellular matrix. Curr. Opin. Cell Biol. 3 800-804. 

FIGURE 15.2 Anti-inflammatory effects exerted by liver X receptor (LXR) agonists on vascular endothelial cells (ECs), smooth muscle cells (SMCs) and macrophages. ABC, ATP-binding cassette transporter ICAM-l, intercellular adhesion molecule-1 VCAM-1, vascular cell adhesion molecule-1 IL, interleukin MMP-9, matrix metaUoprotease-9 COX-2, cyclooxygenase-2 MCP-1, monocyte chemotactic protein-1 iNOS, inducible nitric oxide synthase. 

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