Journal
HUMAN MOLECULAR GENETICS
Volume 29, Issue 2, Pages 335-350Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddz287
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Funding
- National Health and Medical Research Council of Australia
- Shepherd Foundation
- Jack Brockhoff Foundation
- Scobie Trust
- Shane O'Brien Memorial Asthma Foundation
- Our Women's Our Children's Fund Raising Committee Barwon Health
- Rotary Club of Geelong
- Ilhan Food Allergy Foundation
- GMHBA Ltd
- Gandel Foundation
- Percy Baxter Charitable Trust
- Perpetual Trustees
- Gwenyth Raymond Trust
- Victorian Government's Operational Infrastructure Support Program
- NHMRC
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Despite the many advances made in the diagnosis and management of preeclampsia, this syndrome remains a leading cause of maternal mortality and life-long morbidity, as well as adverse fetal outcomes. Successful prediction and therapeutic intervention require an improved understanding of the molecular mechanisms, which underlie preeclampsia pathophysiology. We have used an integrated approach to discover placental genetic and epigenetic markers of preeclampsia and validated our findings in an independent cohort of women. We observed the microRNA, MIR138, to be upregulated in singleton preeclamptic placentas; however, this appears to be a female infant sex-specific effect. We did not identify any significant differentially methylated positions (DMPs) in singleton pregnancies, indicating that DNA methylation changes in mild forms of the disease are likely limited. However, we identified infant sex-specific preeclampsia-associated differentially methylated regions among singletons. Disease-associated DMPs were more obvious in a limited sampling of twin pregnancies. Interestingly, 2 out of the 10 most significant changes in methylation over larger regions overlap between singletons and twins and correspond to NAPRT1 and ZNF417.
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