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

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Published on: January 26, 2024

Endothelial progenitor cells and preeclampsia.

Hilary S Gammill¹, Carol Lin, Carl A Hubel

¹Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.

Frontiers in Bioscience : a Journal and Virtual Library

|November 28, 2006

Summary

In normal pregnancy, maternal endothelial progenitor cells (EPCs) increase to support vascular health. Preeclampsia may involve a failure of this EPC response, potentially due to antiangiogenic factors.

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Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood

Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood

Published on: September 14, 2017

Area of Science:

Reproductive biology
Vascular biology
Maternal-fetal medicine

Background:

Pregnancy involves significant maternal cardiovascular adaptations, including changes in vascular endothelial cells.
Preeclampsia is characterized by multisystemic maternal manifestations linked to vascular endothelial dysfunction.
The mechanisms of normal pregnancy's adaptive endothelial changes and their failure in preeclampsia are not fully understood.

Purpose of the Study:

To investigate the role of endothelial progenitor cells (EPCs) in maternal cardiovascular adaptation during pregnancy.
To explore the potential mechanisms underlying endothelial dysfunction in preeclampsia, focusing on EPCs.

Main Methods:

Review of existing literature on maternal cardiovascular adaptation, endothelial progenitor cells, and preeclampsia.
Analysis of emerging data on EPC populations in the maternal circulation during normal pregnancy and preeclampsia.

Main Results:

Endothelial progenitor cells (EPCs) are mobilized by stimuli like estrogen and vascular endothelial growth factor.
EPCs contribute to endothelial repair and maintenance, acting as a cellular reservoir.
Data suggest maternal EPC circulation increases in normal pregnancy but fails to do so in preeclampsia.

Conclusions:

A deficit in maternal EPC number or activity may contribute to endothelial dysfunction in preeclampsia.
Antiangiogenic factors, such as soluble fms-like tyrosine kinase (sFlt-1) and soluble endoglin, may interfere with EPC function.
Further research is needed to elucidate the precise role of EPCs and antiangiogenic factors in preeclampsia pathogenesis.