Wound healing is a vital physiologic process aimed at reestablishing the integrity of the integument. Activation of the neuroendocrine system by stress has been shown to alter the kinetics of wound healing. Recent studies suggest that stress- induced disturbances of the neuroendocrine equilibrium may provoke alterations in the expression of pro inflammatory cytokines and growth factors that are important in angiogenesis. Angiogenesis, the formation of new blood vessels from preexisting vessels, is essential for the repair, remodeling, and regeneration of damaged tissue. Suppression of pro-angiogenic growth factors may decrease the rate of the neovascularization of granulation tissue, prolonging the proliferative and remodeling phases of wound healing. The purpose of this study is to describe the interrelationships between the neuroendocrine responses, growth factor gene expression, and wound healing in a murine model of restraint stress. We hypothesize that gene expression of the pro-angiogenic growth factors VEGF, FGF-1, and FGF-2 is altered by restraint stress, resulting in slower neovasculaturization of the wound tissue. An elevated level of corticosterone is the underlying factor that contributes to a delay in the neovascularization of the healing wound in restraint stressed animals.
| Horan, Michael P; Quan, Ning; Subramanian, Sukanya V et al. (2005) Impaired wound contraction and delayed myofibroblast differentiation in restraint-stressed mice. Brain Behav Immun 19:207-16 |
