University of Groningen
The effects of preeclampsia on the maternal cardiovascular system
Lip, Simone V.
DOI:
10.33612/diss.130539197
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Publication date: 2020
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
Lip, S. V. (2020). The effects of preeclampsia on the maternal cardiovascular system: Gene expression and its (epigenetic) regulation in experimentel preeclamptic cardiovascular tissues and cells. University of Groningen. https://doi.org/10.33612/diss.130539197
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These propositions belong to the PhD thesis entitled
The effects of preeclampsia on the maternal cardiovascular system
Gene expression and its (epigenetic) regulation in experimental preeclamptic cardiovascular tissues and cells
1. The increased expression of genes encoding for potassium channels in our experimental preeclamptic model is a compensatory mechanism, related to hypertension induced by other mechanisms (This thesis, Chapter 2).
2. If the different epigenetic programs of cardiac tissue during or after experimental preeclampsia as compared with during or after normal pregnancy are also present in humans, this might explain the increased risk of developing heart disease in later life (This thesis, Chapter 3).
3. The increased miR-574-5p and miR-1972 plasma levels during preeclampsia have anti-angiogenic effects and might therefore be key modulators of endothelial dysfunction during preeclampsia (This thesis, Chapter 5).
4. If miR-574-5p and miR-1972 levels are already increased early in pregnancy, these microRNAs may contribute to a better biomarker profile for early preeclampsia diagnostics (This thesis, Chapter 5).
5. Since during preeclampsia many factors are out of balance, an ideal therapeutic intervention would target multiple factors. (This thesis, Chapter 7)
6. Since the concentrations of TNFα, ATP, disulfide HMGB1, microRNAs and others vary between individual preeclamptic patients, personalized medicine might be required to decide which factors should be included in the ideal therapeutic intervention for each patient individually (This thesis, Chapter 7).
7. If the sex-specific gene expression and DNA methylation patterns in fetal endothelial cells remain present in adult life, they may be (partly) responsible for the differences in incidence and
pathogenesis of cardiovascular diseases between sexes (This thesis, Chapter 6). 8. Sex differences are underestimated in cardiovascular diagnostics and therapy.
