Related Experiment Video
Updated: Jun 25, 2026

05:31
Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
Differential placental gene expression in severe preeclampsia
V Sitras1, R H Paulssen, H Grønaas
1Department of Obstetrics and Gynecology, University Hospital of Northern Norway, University of Tromsø, Tromsø, Norway. vasilis.sitras@unn.no
Placenta
|March 3, 2009
Summary
Severe preeclampsia alters placental gene expression, with significant up-regulation of genes like leptin and down-regulation of PDGFD. Early-onset preeclampsia involves distinct pathways like oxidative stress and inflammation.
Area of Science:
- Genomics
- Obstetrics
- Molecular Biology
Background:
- Preeclampsia is a severe pregnancy complication with poorly understood placental pathophysiology.
- Investigating placental gene expression offers insights into disease mechanisms.
Purpose of the Study:
- To comprehensively analyze the global placental gene expression profile in severe preeclampsia.
- To identify differentially expressed genes and associated pathways in preeclampsia.
- To compare gene expression patterns between early- and late-onset preeclampsia.
Main Methods:
- Gene expression profiling using a 30K Human Genome Survey Microarray.
- Analysis of 21 severe preeclamptic placentas and 21 matched controls.
- Empirical Bayes analysis to identify significantly differentially expressed genes (fold-change ≥ 2, p ≤ 0.01).
- Validation using RT-PCR, quantitative urine hCG, and histopathology.
Main Results:
- 213 genes were significantly up-regulated and 82 down-regulated in preeclamptic placentas.
- Key up-regulated genes included leptin, laeverin, beta-hCG isoforms, endoglin, FLT1, and FLT4.
- Down-regulated gene PDGFD was identified.
- Differentially expressed genes were linked to Alzheimer disease, angiogenesis, and Notch, TGFbeta, and VEGF signaling pathways.
- 168 differentially expressed genes distinguished early- from late-onset preeclampsia, implicating oxidative stress, inflammation, and endothelin signaling in early-onset disease.
Conclusions:
- Placental gene expression is significantly altered in severe preeclampsia.
- A comprehensive list of differentially expressed genes provides a resource for further research.
- Distinct placental gene expression profiles suggest different pathophysiological mechanisms for early- and late-onset preeclampsia.
