ABSTRACT
Fibronectin in the skin appears most prominent when adjacent cells are migrating or proliferating. This is true whether embryogenesis, morphogenesis, wound repair, inflammatory conditions, or tumors are being investigated. Although fibronectin appears to have a limited capacity to act directly as and opsonin, fibronectin has been demonstrated to promote opsonic activity of other systems. During granulation tissue formation, fibronectin provides a substrate for cell movement, a chemotactic or haptotic signal for such movement, and a nonspecific opsonin of debris that obstructs such movement. The chemotactic activity of fibronectin fragments for monocytes is reminiscent of the chemotactic activity of collagen and elastin fragments for human monocytes. Extrapolating these data to the skin disorders listed above, it is likely that the increased fibronectin noted within the microvasculature near sites of inflammation is deposited by activated endothelial cells. Preventing formation of a fibronectin matrix by human fibroblasts in vitro inhibits deposition of collagen types I and III.
