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.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Individual Predoctoral NRSA for M.D./Ph.D. Fellowships (ADAMHA) (F30)
Project #
5F30DE005755-04
Application #
6649182
Study Section
Special Emphasis Panel (ZDE1-WG (41))
Program Officer
Hardwick, Kevin S
Project Start
2002-09-01
Project End
2005-08-31
Budget Start
2003-09-01
Budget End
2004-08-31
Support Year
4
Fiscal Year
2003
Total Cost
$30,344
Indirect Cost
Name
Ohio State University
Department
Dentistry
Type
Schools of Dentistry
DUNS #
071650709
City
Columbus
State
OH
Country
United States
Zip Code
43210
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