When human skin is severely wounded, the repair mechanism is notoriously inadequate. The superficial layer, called the epidermis, can re-grow but the underlying tissue, called the dermis, doesn’t remodel and the result is scar tissue. Scar tissue is skin that lacks epithelial appendages (e.g., sweat glands, hair follicles (HF)). Several Wnt genes have been shown to be expressed during wound healing leading to speculation that Wnt factors could be used to stimulate skin healing. In addition; when delivered subcutaneously, purified Wnt3a packaged in liposomal vesicles induce HF neogenesis, demonstrating their robust biological activity in a regenerative context. Using the mouse ear as a model system we aim to gain insights into the mechanism by which Wnt signaling regulates skin healing through the use of the mouse strain Axin2LacZ/LacZ in which the cellular response to Wnt is increased. In parallel, to increase the duration and strength of Wnt signaling at the sites of injury, Wnt3a liposomes will be used to directly evaluate this mode of improved healing. Because Wnt signaling is conserved in mammalian tissue repair, this protein-based approach may have widespread applications in regenerative medicine.