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  • Title: Corticotrophin-releasing factor immunostaining is present in placenta and fetal membranes from the first trimester onwards and is not affected by labour or administration of mifepristone.
    Author: Cooper ES, Brooks AN, Miller MR, Greer IA.
    Journal: Clin Endocrinol (Oxf); 1994 Nov; 41(5):677-83. PubMed ID: 7828359.
    Abstract:
    BACKGROUND AND OBJECTIVES: Corticotrophin releasing factor (CRF) is present in the human placenta and fetal membranes. Placental CRF content and plasma CRF concentrations rise throughout gestation and fall rapidly after delivery. The regulation of CRF production from the placenta is poorly understood. The objective of this study was to use the antiprogestin, mifepristone, to determine whether progesterone has a regulatory effect on CRF production in the first trimester of pregnancy. PATIENTS: Women undergoing first trimester (gestation 5-12 weeks) therapeutic abortion (by suction curettage with and without the synthetic PGE1 analogue, gemeprost (16,16-dimethyl-trans-delta 2-PGE1 methyl ester) vaginally 2-4 hours prior to the procedure; or with 600 mg mifepristone 48 hours prior to receiving 1 mg gemeprost vaginally), second trimester therapeutic abortion (600 mg mifepristone, 1 mg gemeprost), in association with preterm delivery (gestation 25-34 weeks) and at term (gestation 35-42 weeks) by spontaneous delivery, induced labour or elective Caesarean section. MEASUREMENTS: Immunohistochemical localization of CRF and quantification of CRF content by radioimmunoassay of tissue extracts, in human placenta and fetal membranes. RESULTS: CRF was immunolocalized to the syncytiotrophoblast cells of the placenta at all stages of gestation from 5 to 42 weeks. In the fetal membranes CRF immunoreactivity was localized in the epithelial and subepithelial cells of the amnion, some cells of the reticular and cellular layers of the chorion, and in decidual stroma. This pattern was seen in all tissues studied. Pretreatment with prostaglandins, mifepristone or both during the first trimester did not alter the distribution or the intensity of the CRF immunostaining. Placental CRF content rose throughout gestation but, consistent with the immunostaining results, was unaffected by the administration of mifepristone or by labour. CONCLUSIONS: CRF is localized in the syncitiotrophoblast cells of the placenta and is clearly present early in the first trimester of pregnancy. The lack of an effect of mifepristone or mode of delivery suggests that syncytiotrophoblast produces CRF constitutively throughout pregnancy.
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