Chronic wounds are wounds that fail to heal in an orderly set of stages and in a predictable amount of time the way most wounds do. In the U.S., 2% of people suffer from chronic wounds, and nearly 60% of these wounds are caused by infections. Unfortunately, wounds impair quality of life both physically and psychologically, while costing the medical system over $25 billion annually. The faster wound closure occurs, the less likely bacteria will infect the wound, fostering a need for the elucidation of potential biological agents that could accelerate regeneration. Previous studies have identified transforming growth factor-beta (TGF-β) as a protein that plays a critical role in the different phases of wound healing by accelerating the production of the extracellular matrix, which is the cellular network that provides tissue structure, and by inducing the proliferation of different cells such as fibroblasts, which secrete collagen proteins and aid in healing. Adipose-derived stem cells (ASCs) are considered prominent actors as they secrete paracrine factors, or signaling molecules that accelerate healing. TGF-β has been found to induce increased responses in cells such as fibroblasts. However, the potential for TGF-β to stimulate the secretion of paracrine factors such as vascular endothelial growth factor (VEGF), a protein that aids in blood vessel formation, from ASCs, has not been investigated. If TGF-β can upregulate VEGF secretion from ASCs, healing could be drastically accelerated as blood vessels would form faster. Thus, this study aims to determine if TGF-β can induce VEGF secretion from ASCs by comparing VEGF and blood vessel quantity in a control murine model to an experimental group that will receive a topically applied TGF-β culture medium. It is predicted that TGF-β will increase VEGF secretion, creating the possibility that TGF-β-related therapeutic strategies can be developed using data from this proposed research.