F Zhou1, L Zhang2, Q Sun3, X D Wang4. 1. Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, Sichuan 610041, China. 2. Department of Obstetrics and Gynecology, The Peking Union Medical College Hospital, Beijing 100000, China. 3. Reproductive Medicine Center, Nanjing General Hospital of Nanjing Military Command, Nanjing 210000, China. 4. Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, Sichuan 610041, China. Electronic address: wangxd_scu@sina.com.
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 < 0.05). Placental CRH-R2 (0.97 ± 0.09 vs. 0.86 ± 0.09) showed no difference between the ICP and controls (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 < 0.05). Maternal serum UCN levels demonstrated no difference from 34 (79.47 ± 11.35 pg/ml) to 37 (84.24 ± 13.62 pg/ml) weeks of gestation in controls (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 < 0.05) and were lower than controls at 35 (64.19 ± 22.50 pg/ml), 36 (50.06 ± 13.98 pg/ml) and 37 weeks of gestation (all P < 0.05). 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.
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 < 0.05). Placental CRH-R2 (0.97 ± 0.09 vs. 0.86 ± 0.09) showed no difference between the ICP and controls (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 < 0.05). Maternal serum UCN levels demonstrated no difference from 34 (79.47 ± 11.35 pg/ml) to 37 (84.24 ± 13.62 pg/ml) weeks of gestation in controls (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 < 0.05) and were lower than controls at 35 (64.19 ± 22.50 pg/ml), 36 (50.06 ± 13.98 pg/ml) and 37 weeks of gestation (all P < 0.05). 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.