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Related Experiment Video

Updated: Jul 10, 2026

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

Published on: November 8, 2024

Preeclampsia and angiogenic imbalance.

Sharon Maynard¹, Franklin H Epstein, S Ananth Karumanchi

¹Renal Division, Department of Medicine, George Washington University School of Medicine, USA.

Annual Review of Medicine

|October 17, 2007

Summary

Preeclampsia involves placental antiangiogenic factors like soluble Flt1 and soluble endoglin, which cause endothelial dysfunction and pregnancy hypertension. Understanding these factors may improve preeclampsia detection and treatment.

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Last Updated: Jul 10, 2026

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

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Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

Area of Science:

Obstetrics and Gynecology
Maternal-Fetal Medicine
Vascular Biology

Background:

Preeclampsia is a pregnancy syndrome causing endothelial dysfunction, originating in the placenta.
The molecular causes of preeclampsia were unclear until recent focus on placental antiangiogenic factors.

Purpose of the Study:

To explore the role of antiangiogenic factors in preeclampsia pathogenesis.
To investigate the molecular basis of placental dysregulation in preeclampsia.

Main Methods:

Analysis of maternal circulation for antiangiogenic factors.
Exploration of angiogenic proteins in early placental vascular development.

Main Results:

Increased placental antiangiogenic factors (soluble Flt1, soluble endoglin) detected in maternal circulation before preeclampsia onset.
These factors induce systemic endothelial dysfunction, leading to hypertension and proteinuria.

Conclusions:

Altered placental expression of antiangiogenic factors is key to preeclampsia development.
Discoveries offer potential for transforming preeclampsia detection and treatment.