BIGH3 And Its Role In Wound Healing

Accelerated tissue remodeling is a central goal in the fields of wound healing.  Optimal healing reduces post-injury infection and stress, and lowers the costs and productivity associated with poor wound healing. Successful wound healing often involves particular actions of cells including adhesion, migration, synthesis and secretion of new extracellular matrix (ECM) molecules, ECM organization and apoptosis to remove the excess and injured cells.  We are investigating an ECM protein BIGH3 and its roles in wound healing. BIGH3 is a member of the cell adhesion-class family of ECM proteins.  Presently little is actually known about the roles of BIGH3 following tissue injury. To fill this knowledge gap we hypothesize that BIGH3 promotes wound healing by supporting cell adhesion, migration and ECM organization. To test this hypothesis our methods will employ the use of human dermal fibroblasts, human recombinant BIGH3 protein, Transforming Growth Factor-beta (TGF-beta), and an in vitro scratch-wound assay. The scratch-wound assay is well established in the field as a means to establish preliminary results. It can be manipulated regarding cell number, cell substratum, exogenous factors to-be-added, and incubation times. Preliminary Results using non-fibroblast cells indicate that BIGH3 supports cell adhesion and migration, and modulates the fibrillogenesis of type I collagen, which is an important ECM protein in human dermis. We conclude that if we prove our hypothesis correct, then BIGH3, and regulation of its expression through TGF-beta, will be useful therapeutic targets that can promote healing of human dermal injuries.  This work was supported by SALSI and UTSA SURF.