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Biomedical subjects

R M Pratt

Publications and source records attributed to R M Pratt.

104 records · Page 6Linked to original sources
PubMed1975

Epithelial cell death and cyclic AMP increase during palatal development.

Cyclic AMP levels increase abruptly in the secondary palatal shelf (mesenchyme plus a two- to three-cell-layered epithelium) between day 15 and 16 of gestation in the rat embryo. The addition of dibutyryl cyclic AMP to the media in which immature palatal shelves (day 14) are cultured causes a precocious decrease in DNA synthesis, but increased glycoprotein synthesis and epithelial adhesiveness. These changes are most evident in the medial-edge epithelial cells and resemble the developmental events that occur normally on day 15 and 16 during formation of the secondary palate. The initiation of epithelial cell death and adhesiveness in the medial edge of the palatal shelf may be mediated through an increase in cyclic AMP.

Animals↗
PubMedDate not supplied

Retinoic acid alters epithelial differentiation during palatogenesis.

Retinoids are teratogenic in humans and animals, producing a syndrome of craniofacial malformations that includes cleft palate. This study investigates the mechanism through which retinoic acid induces cleft palate. Murine palatogenesis after exposure to retinoic acid in utero is compared to normal development and to alterations observed after exposure in organ culture to retinoic acid or epidermal growth factor (EGF). Human embryonic palatal shelves were placed in the organ culture system and the responses to retinoic acid and EGF were compared to those of the murine palatal shelves. Growth factors play a role in normal development and are found in the embryonic palate. In other cell culture systems, retinoids alter the expression of EGF receptors. Our results suggest that in the medial epithelial cells of the palate, retinoic acid sustains the expression of the EGF receptor and the binding of EGF at a time when the expression in control medial cells has declined, and these control cells subsequently undergo programmed cell death. The continued DNA synthesis, proliferation, survival, and shift in phenotype of the medial cells is believed to interfere with the adhesion and fusion of opposing palatal shelves, resulting in cleft palate.

Cell Death↗