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      Concepts of epithelial-mesenchymal interactions during development: tooth and lung organogenesis.

      Journal of Cellular Biochemistry
      Ameloblasts, cytology, Amelogenin, Animals, Cell Differentiation, DNA, Dental Enamel Proteins, genetics, Epithelium, physiology, Fibroblast Growth Factors, Fibroblasts, Gene Expression Regulation, Glucocorticoids, Humans, Hydrocortisone, Lung, embryology, growth & development, Mesoderm, Nucleic Acid Hybridization, Pulmonary Surfactants, biosynthesis, RNA, Messenger, metabolism, Thyroxine, Tooth

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          Abstract

          One of the major problems in developmental biology concerns how differential gene activity is regionally controlled. One approach to this problem is the use of mesenchyme specification of epithelial-specific gene expression, such as, during tooth morphogenesis or lung morphogenesis. In the example of tooth morphogenesis, dental papilla ectomesenchyme induces de novo gene expression as assayed by detection of amelogenin transcripts, or immunodetection of amelogenin polypeptides within ameloblast cells. This process does not require serum supplementation or exogenous factors during epithelial-mesenchymal interactions in vitro. In contrast, lung morphogenesis requires hormones to mediate mesenchyme-derived influences upon type II epithelial cell differentiation and the production of pulmonary surfactant (eg, neutral and phospholipids, surfactant proteins). Glucocorticoids are required to stimulate the release of fetal pneumonocyte factor (FPF) from fibroblasts which, in turn, enhance the production of pulmonary surfactant. Thyroxin appears to regulate the relative responsiveness of progenitor type II cells to steroid-stimulated release of FPF. This review will highlight key concepts associated with these developing organ systems and emphasize the problem of regional controls which regulate epithelial cell-specific gene activity.

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