Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Sing Sing Way, Cincinatti Children's Hospital, United States
- Second opponent: Team Leader Mads Kamper-Jørgensen, Steno Diabetes Center Copenhagen, Denmark
- Third member and chair of the evaluation committee: Professor Benedicte Alexandra Lie, University of Oslo
Chair of the Defence
Professor II John Torgils Vaage, University of Oslo
Principal Supervisor
Professor Anne Cathrine Staff, University of Oslo
Summary
During pregnancy, fetal cells enter maternal circulation giving rise to fetal microchimerism. These cells remain detectable in the mother for many years after her baby is born. From an evolutionary perspective this phenomenon is likely beneficial: fetal cells persisting in the mother may improve long-term maternal health and enhance survival of the newborn. However, in pregnancies complicated by placental dysfunction, the composition and function of cells transferred to the mother may be altered, thereby conferring harmful effects.
Placental dysfunction may give rise to preeclampsia, gestational diabetes and fetal growth restriction, all of which confer an increased risk of morbidity and mortality in the mother and child. Improving our understanding of the underlying pathophysiology of these conditions is therefore essential. With that aim, the present thesis examines fetal cells in maternal circulation in healthy term pregnancies and pregnancies complicated by new-onset hypertension and diabetes mellitus respectively.
The thesis presents the novel finding that fetal microchimerism in maternal circulation increases in pregnancies where the placenta becomes dysfunctional. We demonstrated that maternal glucose control increases the risk of detecting fetal cells in maternal blood. Furthermore, our findings suggest that fetal cells may play a role in maternal blood pressure elevation in women with preeclampsia. This fits well with the epidemiologically known link between diabetes mellitus and preeclampsia and supports a role for fetal cells in fetal-maternal crosstalk during pregnancy that may have long lasting effects in the mother, given the longevity of these fetal cells.
Whether fetal cells transferred in the setting of placental dysfunction contribute to the known epidemiological link between pregnancy complications and premature maternal cardiovascular disease in the long term is an exciting venue of research that remains to be studied.
Additional information
Contact the research support staff.