Adult-type wound healing has been described as follows. When full-thickness excision wounds are made on the skin of adult mammals, a clot formed by the blood-clotting reaction covers the wounded area, and temporarily shielding the wound from the external environment. Next, cells of the inflammation system such as neutrophils or macrophages move into the corium of the wounded area and multiply. These cells discharge cytokine and other growth factors, and inflammatory reaction occurs in the wounded area. Mast cells play a major role in this inflammatory reaction [16]. As a result, fibroblasts increase in number in the corium of the wounded area. Granulation tissue, which is a transient connective tissue, is formed by fibroblasts discharging abundant extracellular matrixes such as fibronectin or collagen. Granulation tissue is constrictive tissue containing myofibroblasts, and shrinks by the vulnerary last healing process, but leaves a scar. The myofibroblasts disappear from granulation tissue by apoptosis, after the granulation tissue shrinks [6, 8]. The type and expression intension of the proteins in human skin change in each developmental stage, from the fetus to the adult [4]. Furthermore, the type and expression level of the protein in each healing process or in each area vary in the human skin [5]. These reports suggest that the types and expression level of the proteins and the cellular quantity or activity that are associated with them during wound healing may be characteristic structures and functions in adult-type wound healing. Reports suggest that organization of a scar causes differences in the network and accumulation speed of collagen [11, 12].