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  • Title: Inhibition of embryonic palatal shelf horizontalization and medial edge epithelial breakdown by cortisol: role of H-2 in the mouse.
    Author: Goldman AS, Herold R, Piddington R.
    Journal: J Craniofac Genet Dev Biol; 1988; 8(2):135-45. PubMed ID: 3182969.
    Abstract:
    We have investigated the effect of glucocorticoids on the development of the embryonic palate in vivo and of glucocorticoids and diphenylhydantoin (DPH) in culture in the cleft palate-sensitive B10.A strain and its resistant congenic partner strain, B10, as well as the effect of glucocorticoids in vivo in the sensitive A/J strain. The B10.A (H-2a) strain differs from its congenic partner strain, B10 (H-2b), only in the H-2 region of chromosome 17, and thus, differences between the two strains in the responses to the drugs can be ascribed to H-2-linked genes. The degree of corticoid-induced inhibition of shelf horizontalization in vivo is only slightly (if at all) greater in B10.A than in B10, but the degree of corticoid-induced inhibition of fusion following contact in vivo and the inhibition by cortisol and DPH of programmed cell death and breakdown of the medial edge epithelium (MEE) in vitro are much greater in B10.A than in B10. The corticoid-induced delay of shelf horizontalization produced in vivo in the A/J (H-2a) strain is considerably greater than that produced in either B10.A or B10. Thus, H-2-linked genes appear to influence slightly, if at all, the degree of corticoid-induced delay of shelf elevation, but they have a major effect on the corticoid-induced inhibition of fusion via the inhibition of breakdown of the medial edge epithelia. The delay of corticoid-induced shelf horizontalization appears to be a trait influenced primarily by non H-2-linked genes.
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