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Updated: May 10, 2026
The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
Study on the regulation of cell adhesion molecule expression and function in placenta from women with intrahepatic
Qiaoling Du1, Lina Zhou, Kehong Hao
1Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, China.
Intrahepatic cholestasis of pregnancy (ICP) is a common complication of pregnancy manifested as skin pruritus of cholestasis. ICP occurs mainly in the second or third trimester of pregnancy and may cause fetal distress, unexpected intrauterine fetal death and does serious harm to maternal and fetal health. The pathogenesis of ICP is still unclear. In ICP placentas, placental syncytiotrophoblasts are the most direct contact between maternal high bile acid environment and fetus. Our previous study found that in ICP placental syncytiotrophoblasts, both mRNA expression level and protein expression level of vascular cell adhesion molecule-1 (VCAM-1), were significantly elevated. Since VCAM-1 is important in inflammatory injury of lymphocytes, we speculate that ICP pathogenesis may be associated with VCAM-1 up-regulation which may lead to inflammatory injury and cause intrauterine fetal distress, intrauterine fetal death and other adverse outcomes. Elucidation of this mechanism should help reveal the ICP pathogenesis and facilitate the clinical treatment of intrauterine fetal death.
Intrahepatic cholestasis of pregnancy (ICP) is a common complication of pregnancy manifested as skin pruritus of cholestasis. ICP occurs mainly in the second or third trimester of pregnancy and may cause fetal distress, unexpected intrauterine fetal death and does serious harm to maternal and fetal health. The pathogenesis of ICP is still unclear. In ICP placentas, placental syncytiotrophoblasts are the most direct contact between maternal high bile acid environment and fetus. Our previous study found that in ICP placental syncytiotrophoblasts, both mRNA expression level and protein expression level of vascular cell adhesion molecule-1 (VCAM-1), were significantly elevated. Since VCAM-1 is important in inflammatory injury of lymphocytes, we speculate that ICP pathogenesis may be associated with VCAM-1 up-regulation which may lead to inflammatory injury and cause intrauterine fetal distress, intrauterine fetal death and other adverse outcomes. Elucidation of this mechanism should help reveal the ICP pathogenesis and facilitate the clinical treatment of intrauterine fetal death.
