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 animals^1–4. Various inbred strains of mice exhibit different degrees of susceptibility to glucocorticoid-induced cleft palate^5–8. 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 proteins^9–11, 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.