At sites of tissue injury or inflammation, extravasation of plasma proteins leads to the formation of a complex fibrillar matrix composed primarily of fibrin and plasma fibronectin (pFN). This protein meshwork serves not only to reestablish the integrity of the vascular system but also to provide a scaffold for cell migration and subsequent wound repair. The interactions between cell surface receptors and this provisional extracellular matrix (ECM) provide important cues that can modulate the cellular response at the injury site, leading to alterations in cell growth and gene expression. Key determinants of this response may lie in the structure and composition of this "injury-associated" ECM.