Fig. 2.

A summary comparison of skin injury response in mammals versus axolotls. (A). In mammalian wound healing, a fibrin clot is formed, and keratinocytes will proliferate and migrate under the clot. As keratinocyte migration is occurring, fibroblasts will enter into the wound bed and proliferate, and will start to express extracellular matrix (ECM) proteins such as collagen. Once there is a provisional matrix, keratinocytes can migrate over to close the wound. Some fibroblasts will differentiate into myofibroblasts and will contract the wound. Scar formation is the result of mammalian wound healing, marked by a thickened epidermis, as well as excessive and un-remodeled collagen deposition. (B). In axolotl wound healing, keratinocytes will migrate over the fibrin clot, closing the wound within 24 h. Once the wound is closed, the keratinocytes will proliferate, and create a wound epidermis. Fibroblasts will enter the wound bed, proliferate, and secrete ECM. Again, some of the fibroblasts will differentiate into myofibroblasts and contract the wound. The cells within the dermis will then continue to remodel the ECM that was deposited until regeneration has been achieved.