Glucocorticoids increase pulmonary epidermal growth factor receptors in female and male fetal rabbit.
Experimental evidence in animals and humans suggest that glucocorticoids enhance fetal pulmonary maturation. Mechanisms of glucocorticoid effects remain unclear; but apparently include up regulation of fetal pulmonary insulin and beta-adrenergic receptors. A role of Epidermal Growth Factor (EGF) in fetal lung maturation through plasma membrane bound receptors has been recently proposed. Betamethasone, 0.085 mg/kg, was administered on 25th and 26th day of gestation to the rabbit doe. Fetal pulmonary EGF receptor characteristics in male or female fetuses were studied on the 27th day of pregnancy. The percent specific binding of 125-I-EGF to lung plasma membranes (LPM) and the number of receptor sites per mg of LPM protein or DNA content were significantly higher in the glucocorticoid treated female as well as male fetuses when compared to the control pups, with no difference in the Kd. Presence of high affinity receptors for EGF and their up regulation by glucocorticoids support the hypothesis that EGF plays an important role in fetal lung maturation and that some of the beneficial effects of glucocorticoids in decreasing the incidence of HMD may be mediated through its interaction with EGF.
D000818:Animals; D001623:Betamethasone / Q000494:pharmacology*; D002462:Cell Membrane / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004815:Epidermal Growth Factor / Q000378:metabolism; D066246:ErbB Receptors; D005260:Female; D008168:Lung / Q000196:embryology* / Q000378:metabolism; D008297:Male; D011247:Pregnancy; D011817:Rabbits; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*
D011956:Receptors, Cell Surface; D004815:Epidermal Growth Factor; D004247:DNA; D001623:Betamethasone; D066246:ErbB Receptors