It is known that in diabetic ulcers, the increased inflammatory response increases proteolytic activity, or the degradation of proteins. This inhibits target pathways and thereby reduces the production of intracellular growth factors including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). VEGF and bFGF cause capillary formation and are key in the initiation of the process of angiogenesis. Angiogenesis, or vascular tissue formation, is a crucial process in tissue repair and wound-healing, and is stimulated by both the production of these intracellular growth factors, and cell migration towards the wound site. This angiogenic response that occurs immediately following wound formation is caused by an endogenous electric field that develops across tissue layers and triggers wound healing cellular pathways.
Our experiment will use an external electrical stimulus to activate these cellular pathways associated with tissue repair, therefore promoting the rapid healing of the ulcer. Our motivation for the use of electrical stimulation is due to its positive interactions with the human body’s endogenous bioelectric healing system to heal injuries. We believe that electrical stimulation will activate these cellular healing pathways because previous studies have shown that applied current enhances ion transport through the wound and increases cell migration. Other studies have also shown that sensory electrical stimulation is able to release more levels of VEGF in skin, which will improve the healing pathways in diabetic ulcers.
- We aim to examine the effects of an optimized linearly applied electric field on cell proliferation, VEGF expression, bFGF expression and cell migration rates.
- We aim to examine the effects of an optimized radially applied electric field on cell proliferation, the VEGF expression, bFGF expression and cell migration rates.
- We aim to demonstrate that the application of a radial or linear electric field in a designed prototype will reduce chronic inflammation in diabetic ulcers with a diabetic rat model.