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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Full Professor Marc E.A. Spaanderman, Maastricht University, The Netherlands
- Second opponent: Professor with Tenure Nardhy Gomez-Lopez, Wayne State University, USA
- Third member and chair of the evaluation committee: Professor Benedicte Alexandra Lie, University of Oslo
Chair of the Defence
Professor Emeritus Ingebjørg Seljeflot, University of Oslo
Principal Supervisor
Professor Anne Cathrine Staff, University of Oslo
Summary
Preeclampsia, a hypertensive disorder of pregnancy, confers increased risk of future maternal cardiovascular disease. The mechanisms are largely unknown. Foam cell lesions (acute atherosis) of placenta-supplying decidua basalis spiral arteries, resembling early atherosclerotic lesions, are frequent in preeclampsia. The thesis aimed to study molecular features associated with atherosclerosis both in preeclampsia and in acute atherosis, in order to uncover potential shared mechanisms between these arterial diseases. Biosamples from pregnant women were collected prior to or at caesarean delivery. Decidua basalis tissue was stained with immunohistochemistry, maternal blood was analyzed by enzyme-linked immunosorbent assay, to study vascular and circulating biomarkers in preeclampsia and acute atherosis. Acute atherosis endothelium is damaged, but not activated, differing from atherosclerosis. Acute atherosis foam cells express similar proteins as those in atherosclerosis. Circulating protein misfolding markers are dysregulated (as in atherosclerosis) in women with preeclampsia delivered early preterm and in placental dysfunction, but not in acute atherosis. The thesis uncovered shared and differing local and systemic molecular biomarkers in preeclampsia, acute atherosis, and atherosclerosis.
Additional information
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