Bile acid signaling in fetal tissues: implications for intrahepatic cholestasis of pregnancy

Catherine Williamson, Michele Miragoli, Siti Sheikh Abdul Kadir, Shadi Abu-Hayyeh, Georgia Papacleovoulou, Victoria Geenes, Julia Gorelik

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)


Background/Aims: Intrahepatic cholestasis of pregnancy (ICP) is complicated by spontaneous preterm labor, fetal anoxia and unexplained fetal death. We aim to evaluate the mechanisms by which raised fetal bile acids cause placental abnormalities and fetal cardiac pathology. Methods: The study was performed using placental samples taken from ICP pregnancies, placental explant culture, neonatal and adult cardiomyocytes, and murine and human embryonic stem cell-derived cardiomyocytes. Results: Maternal cholestasis causes a placental phenotype with histological abnormalities. This can be evaluated using placental explant cultures. Taurocholate, the principal bile acid raised in the fetal compartment in ICP, causes abnormal cardiomyocyte contraction, rhythm and desynchronization of calcium dynamics. To extend our observations that the muscarinic M2 receptor plays a role in bile acid-induced arrhythmia in cardiomyocytes, we are developing a model containing mixed cell populations to represent the fetal and maternal hearts. This will be used to evaluate the underlying mechanisms to explain fetal arrhythmia in the presence of cholestasis. Conclusion: Bile acids signal via a spectrum of pathways in the placenta and the fetal heart.
Original languageEnglish
Pages (from-to)58-61
Number of pages4
JournalDigestive diseases (Basel, Switzerland)
Issue number1
Publication statusPublished - Jun 2011


  • Maternal-Fetal Exchange
  • Fetus
  • Pregnancy Complications
  • Cholestasis, Intrahepatic
  • Fetal Heart
  • Bile Acids and Salts
  • Humans
  • Signal Transduction
  • Female
  • Pregnancy


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