Mechanisms by which fibrin and fibronectin appear in healing wounds: implications for Peyronie's disease.

Abstract

The extracellular matrix that is present at sites of tissue repair in most instances undergoes an orderly transition from a fibrin containing matrix to collagen-rich scar. However, in some conditions, such as Peyronie's disease, fibrin persists. Evidence from a number of experimental systems indicates that extracellular matrix proteins and their receptors serve an important function in regulating cell behaviors. Thus, the presence of the fibrin matrix is likely to have important implications in the course of either normal or pathogenic wound healing as occurs in Peyronie's disease. Potential mechanisms by which the fibrin rich provisional matrix appears in healing wounds are presented. Methodologies, such as in situ hybridization, immunolocalization and labeled tracer techniques, were used in our study. We found by these approaches that the 2 general mechanisms that contribute to the generation of the wound extracellular matrix are leakage of plasma proteins, such as plasma fibronectin and fibrinogen, and the synthesis of variants of fibronectin by wound cells. Developing an understanding of the mechanisms that regulate the appearance of these matrix proteins may provide new avenues for therapy in conditions such as Peyronie's disease in which the temporal pattern of the provisional matrix deposition is abnormal.