Related Experiment Video
Updated: Sep 28, 2025
Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
Published on: July 30, 2016
Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress Associated with Preeclampsia
Gina D Kusuma1,2, Harry M Georgiou1,2, Anthony V Perkins3
1The University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Parkville, Victoria, Australia.
Insights
Preeclampsia (PE) involves pregnancy-induced hypertension and proteinuria. This review explores how mesenchymal stem/stromal cells (MSC) respond to oxidative stress in PE, suggesting therapeutic manipulation as a potential treatment.
Area of Science:
- Obstetrics and Gynecology
- Maternal-Fetal Medicine
- Stem Cell Biology
Background:
- Preeclampsia (PE) is a critical pregnancy disorder characterized by new-onset hypertension and proteinuria.
- Placental dysfunction in PE leads to altered angiogenic factor secretion and maternal vascular endothelial damage.
- The decidua, a major source of oxidative stress in PE, contains mesenchymal stem/stromal cells (MSC) whose role is unclear.
Purpose of the Study:
- To review the response of decidua-derived MSC to oxidative stress in normal pregnancy and PE.
- To investigate the compromised biological mechanisms of MSC in response to oxidative stress in PE.
- To explore the therapeutic potential of modulating MSC oxidative stress response for PE treatment.
Main Methods:
- Review of existing literature on MSC biology and oxidative stress.
- Analysis of MSC responses in normotensive versus preeclamptic pregnancies.
- Discussion of potential therapeutic strategies targeting MSC in PE.
Main Results:
- MSC possess a universal ability to respond to oxidative damage.
- These MSC response mechanisms are compromised in the context of preeclampsia.
- Abnormal MSC function contributes to maternal vascular endothelium damage in PE.
Conclusions:
- Understanding MSC oxidative stress response is crucial for deciphering PE pathogenesis.
- Targeting the aberrant oxidative stress response of MSC presents a potential therapeutic avenue for preeclampsia.
- Further research into MSC manipulation could lead to novel treatments for PE beyond delivery.
Abstract:
Preeclampsia (PE) is a serious medically important disorder of human pregnancy, which features de novo pregnancy-induced hypertension and proteinuria. The severe form of PE can progress to eclampsia, a convulsive, life-threatening condition. When placental growth and perfusion are abnormal, the placenta experiences oxidative stress and subsequently secretes abnormal amounts of certain pro-angiogenic factors (eg, PlGF) as well as anti-angiogenic factors (eg, sFlt-1) that enter the maternal circulation. The net effect is damage to the maternal vascular endothelium, which subsequently manifests as the clinical features of PE. Other than delivery of the fetus and placenta, curative treatments for PE have not yet been forthcoming, which reflects the complexity of the clinical syndrome. A major source of reactive oxygen species that contributes to the widespread maternal vascular endothelium damage is the PE-affected decidua. The role of decidua-derived mesenchymal stem/stromal cells (MSC) in normotensive and pathological placenta development is poorly understood. The ability to respond to an environment of oxidative damage is a "universal property" of MSC but the biological mechanisms that MSC employ in response to oxidative stress are compromised in PE. In this review, we discuss how MSC respond to oxidative stress in normotensive and pathological conditions. We also consider the possibility of manipulating the oxidative stress response of abnormal MSC as a therapeutic strategy to treat preeclampsia.
