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Retinoic acid alters epithelial differentiation during palatogenesis
1Experimental Teratogenesis Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27711.
Journal of Craniofacial Genetics and Developmental Biology
|October 1, 1991
Summary
Retinoic acid causes cleft palate by disrupting normal cell death in the developing palate. It sustains epidermal growth factor (EGF) receptor expression, preventing programmed cell death and interfering with palatal shelf fusion.
Area of Science:
- Developmental Biology
- Teratology
- Molecular Biology
Background:
- Retinoids are known teratogens causing craniofacial malformations, including cleft palate.
- The precise molecular mechanisms by which retinoids induce cleft palate are not fully understood.
Purpose of the Study:
- To investigate the mechanism of retinoic acid-induced cleft palate.
- To compare the effects of retinoic acid and epidermal growth factor (EGF) on palatal development in murine and human organ cultures.
Main Methods:
- Comparative analysis of murine palatogenesis following in utero retinoic acid exposure.
- Organ culture of murine and human embryonic palatal shelves exposed to retinoic acid or EGF.
- Examination of EGF receptor expression and cell behavior in medial epithelial cells.
Main Results:
- Retinoic acid sustains EGF receptor expression and EGF binding in medial palatal epithelial cells.
- Control medial cells exhibit declining EGF receptor expression and undergo programmed cell death.
- Sustained proliferation and survival of medial cells due to retinoic acid interfere with palatal shelf adhesion and fusion.
Conclusions:
- Retinoic acid induces cleft palate by altering programmed cell death pathways in medial palatal epithelial cells.
- The sustained expression of EGF receptors by retinoids plays a critical role in this teratogenic effect.
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