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Autophosphorylation of the epidermal growth factor (EGF) receptor in A-431 cells and plasma membrane fractions was inhibited by partially purified recombinant human Müllerian Inhibiting Substance (MIS). Immunoprecipitation of the EFG receptor using anti-EGF receptor or anti-phosphotyrosine antibodies, and phosphoamino acid analysis of this receptor, demonstrated that MIS specifically inhibited EGF-induced tyrosine phosphorylation. Inhibition of EGF receptor autophosphorylation by MIS in membrane preparations was not affected by increasing concentrations of EGF, manganese or [gamma-(32)P] ATP. Thus, it is unlikely that MIS competes for EGF binding sites or sequesters substrate. Immunoabsorption of MIS with anti-human MIS antibody blocked the MIS inhibition of EGF receptor autophosphorylation, indicating that the inhibition was due to MIS. Our data suggest that MIS regulates the activity of the EGF receptor tyrosine kinase in A-431 cells.

Eighteen patients with a prenatal diagnosis of fetal abdominal wall defect were delivered by cesarean section and repaired either immediately (begun within 15 min, n = 9), or by the traditional (delayed) method (n = 9, average delay = 4.4 h). Neonates repaired immediately had comparable gestational ages and birthweight, however, subjectively had less edematous bowel with less fibrous peel. These fetuses were more likely to be closed primarily (7/9 vs. 4/9), spent less time on a ventilator (8.1 vs. 17.9 days), seemed to be fed sooner (7.6 vs. 17.9 days), and discharged home earlier (14.3 vs. 24.0 days). Our results suggest that for fetuses delivered by cesarean section, early defect repair may reduce bowel edema and fibrous peel formation thus facilitating primary closure, with earlier ventilator weaning, feeding and discharge home.

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