Abstract
Fibronectin (FN) is an extracellular matrix protein that acts as a substrate for cell migration and adhesion during development. FN adheres to cells through a dimeric membrane protein, the FN receptor. Antibodies to FN and synthetic peptides that inhibit FN-receptor interaction inhibit gastrulation, block neural crest cell migration, arrest cardiac development, and block the fusion of myoblasts to form myotubes. FN and its receptor also appear to be important for lung development, where their expression coincides with the onset of branching morphogenesis, but drops to barely detectable levels in adult lung, indicating developmental specificity. FN expression is generally low in most adult tissues. However, synthesis is drastically increased during injury and wound healing, a process that in many ways mimics development. FN synthesis is also drastically increased in fibroproliferative lung lesions associated with major architectural changes in the lung. Expression of FN is regulated by a variety of growth factors and hormones. Several of these inducers (cAMP, transforming growth factor-beta, epidermal growth factor, platelet-derived growth factor, glucocorticoids, and vitamin D3) have themselves been implicated in developmental processes, and both cAMP and transforming growth factor-beta are known to stimulate expression of other matrix genes. One role of these hormones and growth factors in development may be to control expression of matrix genes, thereby controlling cell migration and adhesion. In the following report, the effect of hormones and growth factors on expression of the FN gene is reviewed.