RESUMEN
BACKGROUND: Allogeneic skin grafts onto C57BL/6 mice are rejected, and the rejected skin is replaced by surrounding skin with black hair. In contrast, syngeneic skin grafts are tolerated, and gray hair grows on the grafts. METHODS: To explore the mechanism of gray hair growing on the tolerated skin grafts, we prepared full-thickness skin (2-cm square) autografts, 2 (2 cm + 2 cm) horizontal or vertical parallel incisions, and U-shaped (2 cm × 2 cm × 2 cm) flaps with or without pedicle vessels. The grafts, incisions, and flaps were fixed by suturing with string and protected by a transparent bandage. On day 14 after the operation, the bandages were removed to observe the color of the hair growing on the skin. RESULTS: Skin autografts from wild-type or hepatocyte growth factor-transgenic (Tg) C57BL/6 mice survived with gray hair, whereas those from steel factor (Kitl)-Tg C57BL/6 mice survived with black hair. In addition, U-shaped flaps lacking both of the 2 main feeding vessels of wild-type mice had gray hair at the tip of the flaps. Light microscopy after staining with hematoxylin and eosin or dihydroxyphenylalanine showed that the formation of melanin pigment in the follicles, but not in the interadnexal skin, was susceptible to the blood supply. CONCLUSIONS: Melanin pigment formation in the hair bulb melanocytes appeared to be susceptible to the blood supply, and melanocytosis was promoted in the follicles and in the epidermis of Kitl-Tg C57BL/6 mice.
RESUMEN
Tenascin-W is a tenascin family member that forms part of a complex extracellular matrix, and previous studies have suggested its association with osteogenesis. In the present study we investigated the roles of tenascin-W in osteogenesis. We found that tenascin-W is expressed in osteoblasts at the edge of the developing bone domain prior to mineralization in mouse fetuses. Expression of tenascin-W was induced during the course of mineralization of the Kusa-A1 osteoblast cell line. In the interfrontal suture of postnatal mice, the anterior portion remains patent and the posterior portion closes by 4 weeks of age. Tenascin-W expression was downregulated at 1 week of age in the posterior frontal suture, whereas in the anterior suture, expression was maintained until the mice reached 4 weeks of age. Fibroblast growth factor 2 (FGF2)-bead application to the mouse fetal skull by ex-utero surgery accelerated osteoblast differentiation, but inhibited mineralization with a downregulation of tenascin-W expression. These results suggest that tenascin-W is involved in osteoblast maturation (i.e. mineralization).