Glucocorticoid receptors in murine embryonic facial mesenchyme cells.

Abstract

IN various experimental animals, clefting of the developing secondary palate can be induced by the administration of glucocorticoids to pregnant animals1–4. Various inbred strains of mice exhibit different degrees of susceptibility to glucocorticoid-induced cleft palate5–8. Specifically, A/J mice treated with glucocorticoids between days 11 and 14 of gestation (day of detection of vaginal plug designated day 0 of pregnancy) produce 100% of their offspring with cleft palate, whereas C57BL/6J (C57) mice similarly treated produce off spring with only 20–25% cleft palate. Although it has been demonstrated that glucocorticoids can elicit divergent physiological responses in various differentiated cell types through a class of specific cytoplasmic and nuclear receptor proteins9–11, the exact molecular mechanism(s) by which glucocorticoids function as teratogens as well as the aetiology of the strain-specific difference in the response to glucocorticoids are unknown. We present here evidence that mouse facial mesenchyme cells obtained either directly or in primary culture possess specific glucocorticoid-receptor proteins of high affinity and limited capacity for dexamethasone. Furthermore, we report that A/J facial mesenchyme cells possess approximately double the amount of receptor proteins than C57 mesenchyme cells.