Expression of urocortin and corticotrophin-releasing hormone receptor-2 in patients with intrahepatic cholestasis of pregnancy

Abstract Introduction Intrahepatic cholestasis of pregnancy (ICP) is associated with an increased risk of adverse pregnancy outcomes. Fetal distress in ICP is an acute process, and the abnormal expression of placental local vasodilatory factors play an essential role. Urocortin (UCN) exhibits a powerful concentration-dependent vasodilatation effect in the utero-placental-fetal unit. Our study aimed to investigate placental and serum UCN expression in ICP patients. Methods Blood and placenta samples were obtained from the ICP patients and controls. UCN and corticotrophin-releasing hormone receptor-2 (CRH-R2) expression were detected by ELISA, immunohistochemistry, Western Blotting and real-time PCR. Results Placental UCN expression of ICP was lower compare to the controls (0.27 ± 0.11 vs. 0.85 ± 0.21) ( P P  > 0.05). Placental UCN mRNA (1.45 ± 0.31 vs. 0.72 ± 0.29) and CRH-R2 mRNA expression (1.11 ± 0.10 vs. 0.84 ± 0.24) were higher compared to the controls (all P P  > 0.05). Maternal serum UCN levels of ICP were decreased from 34 (68.53 ± 16.95 pg/ml) to 37 (47.91 ± 15.65 pg/ml) weeks of gestation ( P P Discussion The down-regulated UCN expression in the placenta and maternal serum during ICP may impair the blood flow regulation of the utero-placental-fetal unit and contribute to fetal distress. Maternal serum UCN levels might represent a potential clinical predictor of adverse fetal outcomes and optimize the clinical management.