Foetal rat skin rapidly closes an open
wound in organ culture and in vivo, this possibly being unique to organs still in the morphogenetic stage. In the present study, examination was made of morphological changes in foetal rat skin during closure of open
wounds inflicted at day 16 of gestation. Phase-contrast microscopy of open-wounded skin cultured in vitro indicated inward spreading of the peripheral skin to be responsible for
wound closure.
Wound closure in vitro was inhibited by
cytochalasin B (10 micrograms/ml), not by
hydroxyurea (2 mM), indicating prenatal
wound closure to be mediated by regulation of the microfilament system rather than cell proliferation. During
wound closure in vitro and in vivo, light and scanning electron microscopy of the peripheral skin showed cells in the periderm, the outermost layer of the foetal epidermis, to elongate centripetally and en masse, whereas the shape of underlying epidermal cells not to change. Numerous spindle-shaped cells and fibrous matrices in the mesenchyme were redistributed, becoming oriented along the
wound edge. Following isolation of the mesenchyme and epidermis by treatment with
Dispase and separate culturing, the capacity for
wound closure in vitro was found to be retained only by the mesenchyme. Cellular activity within the mesenchyme, rather than in the epidermis, would thus appear essential to
wound closure in foetal rat.