Department of Laboratory Medicine, Laboratory of Genetic, Endocrine and Metabolic Diseases, Radboud University Nijmegen Medical Centre, Geert Grooteplein 8, Nijmegen, the Netherlands.
Placenta. 2010 Jun;31(6):475-81. doi: 10.1016/j.placenta.2010.03.012. Epub 2010 May 6.
Placental urocortins may affect uterine quiescence by modulating in an endocrine or paracrine way the estradiol secretion by the adjacent placenta. The aim of this study was to investigate the role of placental urocortin-2 and -3 as endocrine or as auto/paracrine messengers in concert with placental estradiol generation.
In a cross-sectional study, plasma was obtained from healthy pregnant women, between 10 and 42 gestational weeks, and from nonpregnant women. Third trimester plasma pools were used for urocortin-2 and -3 peptide characterization by HPLC and RIA. Plasma samples (gestational age 10 and 42 wk) were analyzed using validated radioimmunoassays specific for urocortins and corticotropin-releasing factor (CRF). To reveal possible local actions of urocortins the influence of urcortin-2 on the estradiol secretion from placental tissue cultures was investigated.
Reversed-phase HPLC fractionation of plasma extracts revealed several peaks containing immunoreactive-like urocortin-2 or -3, of which the main peaks had the same retention time as the synthetic urocortin-2 or -3 peptides. In contrast to plasma CRF, no gestational age dependent changes in plasma urocortin-1, -2 and -3 levels occurred. The mean plasma urocortin levels during gestation did not differ from postpartum levels. In vitro, urocortin-2 stimulated dose-dependently the placental estradiol secretion, a stimulation inhibited by antisauvagine-30, a CRF-receptor 2 antagonist.
Placentas of healthy pregnant women do not, or not to any great extent, secrete urocortin-2 and -3 in the plasma. We show that urocortins can regulate the estradiol secretion from placental tissue cultures via the CRF-R2 mediated pathway. Therefore, placental urocortin-2 and -3 peptides are more likely to function as auto/paracrine messengers during healthy pregnancy, than as endocrine messengers.
胎盘尿皮质素可能通过内分泌或旁分泌方式调节邻近胎盘的雌二醇分泌，从而影响子宫静止。本研究旨在探讨胎盘尿皮质素-2 和 -3 作为内分泌或自分泌/旁分泌信使与胎盘雌二醇生成协同作用的作用。
在一项横断面研究中，从 10 至 42 孕周的健康孕妇和非孕妇中获得血浆。使用 HPLC 和 RIA 对第三孕期血浆池进行尿皮质素-2 和 -3 肽特征分析。使用针对尿皮质素和促肾上腺皮质释放因子 (CRF) 的经过验证的放射免疫分析，分析妊娠 10 周和 42 周的血浆样本。为了揭示尿皮质素的可能局部作用，研究了尿皮质素-2 对胎盘组织培养中雌二醇分泌的影响。
血浆提取物的反相 HPLC 分级分离显示出几种含有免疫反应性类似尿皮质素-2 或 -3 的峰，其中主要峰的保留时间与合成的尿皮质素-2 或 -3 肽相同。与血浆 CRF 不同，血浆尿皮质素-1、-2 和 -3 水平没有随妊娠年龄的变化而变化。妊娠期间的平均血浆尿皮质素水平与产后水平无差异。在体外，尿皮质素-2 以剂量依赖性方式刺激胎盘雌二醇分泌，该刺激被 CRF 受体 2 拮抗剂抗 Sauvagine-30 抑制。
健康孕妇的胎盘在血浆中不分泌或不大量分泌尿皮质素-2 和 -3。我们表明，尿皮质素可以通过 CRF-R2 介导的途径调节胎盘组织培养中的雌二醇分泌。因此，胎盘尿皮质素-2 和 -3 肽在健康妊娠期间更可能作为自分泌/旁分泌信使发挥作用，而不是作为内分泌信使。
