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Receptor-dependent mechanisms of glucocorticoid and dioxin-induced cleft palate

Journal Article · · Environ. Health Perspect.; (United States)
DOI:https://doi.org/10.1289/ehp.856135· OSTI ID:6023350
Glucocorticoids (triamcinolone) and dioxins (TCDD) are highly specific teratogens in the mouse, in that cleft palate is the major malformation observed. Glucocorticoids and TCDD both readily cross the yolk sac and placenta and appear in the developing secondary palate. Structure-activity relationships for glucocorticoid- and TCDD-induced cleft palate suggest a receptor involvement. Receptors for glucocorticoids and TCDD are present in the palate and their levels in various mouse strains are highly correlated with their sensitivity to cleft palate induction. Receptors for glucocorticoids appear to be more prevalent in the palatal mesenchymal cells whereas those for TCDD are probably located in the palatal epithelial cells. Glucocorticoids exert their teratogenic effect on the palate by inhibiting the growth of the palatal mesenchymal cells whereas TCDD alters the terminal cell differentiation of the media palatal epithelial cells. 71 references.
Research Organization:
National Institute of Environmental Health Sciences, Research Triangle Park, NC
OSTI ID:
6023350
Journal Information:
Environ. Health Perspect.; (United States), Journal Name: Environ. Health Perspect.; (United States) Vol. 61; ISSN EVHPA
Country of Publication:
United States
Language:
English