Study on relationship between expression of familial intrahepatic cholestasis 1 mRNA in placenta and Intrahepatic cholestasis of pregnancy
Objective: By detecting the expression of placental familial intrahepatic cholestasis 1 (FIC1) and levels of total bile acids (TBA) and cholylglycine (CG) in maternal and umbilical cord serum, the effect of placental bile salt transporter on fetal pathology of intrahepatic cholestasis of pregnancy (ICP) is explored.
Methods: TBA and CG levels in maternal and umbilical cord serum of 20 gravidas complicated with ICP (ICP group) and 20 normal gravidas (control group) of late pregnancy were measured by velocimetry and radioimmunoassay respectively. The placental FIC1 mRNA expression was tested by real time RT-PCR. Meanwhile FIC1 mRNA expression of 4 random placentas were localized by in-situ hybridization. RESULTS (1) TBA and CG levels in both maternal and umbilical cord serum of ICP group were significantly higher than those of control group (P < 0.05). TBA and CG levels in maternal serum were significantly higher than those in umbilical cord serum of ICP group (25.77 +/- 16.64) micromol/L vs (8.55 +/- 5.48) micromol/L for TBA, and (3416.09 +/- 1986.04) microg/dL vs (821.84 +/- 673.17) microg/dL for CG, P < 0.05). However, there were no significant differences between TBA and CG levels in maternal serum and umbilical cord serum from control group (3.4 +/- 2.51) micromol/L vs (4. 36 +/- 3. 26) micromol/L for TBA, and (342.74 +/- 234.88) microg/dL vs (309.32 +/- 145.20) pg/dL for CG, P > 0.05). (2) FIC1 mRNA was expressed and localized to syncytiotrophoblast in both ICP and control placentas. Placental FIC1 mRNA expression was significantly decreased in ICP group than in control group (P < 0.05). (3) There were no significant correlations between TBA and CG levels of maternal or umbilical cord serum and expression of placental FIC1 mRNA in both groups (r = -0.229-0.163, P > 0.05).
Conclusions: Our research results suggest that the decreased expression of FIC1 mRNA in placenta may be one of actor of disturbing placental bile salt transport and resulting in fetal cholestasis in ICP.