P-selectin and wound healing

The history of the wound can by some accounts be traced nearly 5,000,000 years in the prehistoric ancestry of man (Majno, 1991). While there have been many descriptive accounts of the wound and wound healing over the centuries, in recent years rapid advances in the field of adhesion biology have added greatly to the understanding of the wound. Disruptions in the continuity of the vessel wall, whether by trauma or disease, induce a number of physiologic responses. The endothelium responds to fibrin contact in numerous ways including the rapid release of stored of von Willebrand factor and the expression of P-selectin upon the cell surface. Deposition of fibrin at the site of vascular injury serves other vital roles in the acute response to injury. Fibrin deposition stabilizes platelets as part of the development of a mural thrombus. Fibrin may also act to serve as a biological scaffold upon which inflammatory cells may adhere and participate in the acute response to injury. Finally, it is apparent that fibrin may act as a lattice upon which fibroblasts, smooth muscle cells and endothelial cells may adhere and migrate in order to return the vessel to its original state. In tumorigenesis, fibrinogen and fibrin may deposit in the perivascular space within the tumor and contribute by incompletely understood mechanisms to tumor growth and metastasis. The understanding of fibrin induced endothelial cell responses and how P-selectin and other endothelial cell adhesion molecules function in wound healing is important for understanding the vascular response to injury.