When skin is damaged, the body releases EGF into the area. The presence of EGF attracts nearby connective tissue cells called fibroblasts. The EGF then signals the fibroblasts to begin producing collagen in the area of the wound to build the foundation of new skin tissue.
Under normal circumstances, the body can use this process to heal a wound. But in the case of chronic wounds, as they occur in diabetics, the lesions remain open. In the past, EGF was applied directly to a wound, but the approach was not successful because small polypeptides such as EGF only remain in the wound site for several minutes before they are dispersed. This is not enough time to rebuild tissue.
MIT and Stanford inventors have developed EGF variants with significantly increased binding affinity to the EGF receptor so that the residence time of EGF will be remarkably prolonged and the biological effect enhanced.
A mutant EGF that stimulates cell cycle progression can, thus, be used as a wound healing agent by accelerating and improving the rate and extent of healing. Furthermore, EGF mutants can influence cell migration in vitro
and in vivo
and so aid wound healing.