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Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress Associated with Preeclampsia
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 plac...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
YJBM
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8961706/ https://www.ncbi.nlm.nih.gov/pubmed/35370491 |
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author | Kusuma, Gina D. Georgiou, Harry M. Perkins, Anthony V. Abumaree, Mohamed H. Brennecke, Shaun P. Kalionis, Bill |
author_facet | Kusuma, Gina D. Georgiou, Harry M. Perkins, Anthony V. Abumaree, Mohamed H. Brennecke, Shaun P. Kalionis, Bill |
author_sort | Kusuma, Gina D. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8961706 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | YJBM |
record_format | MEDLINE/PubMed |
spelling | pubmed-89617062022-03-31 Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress Associated with Preeclampsia Kusuma, Gina D. Georgiou, Harry M. Perkins, Anthony V. Abumaree, Mohamed H. Brennecke, Shaun P. Kalionis, Bill Yale J Biol Med Review 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. YJBM 2022-03-31 /pmc/articles/PMC8961706/ /pubmed/35370491 Text en Copyright ©2022, Yale Journal of Biology and Medicine https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed under the terms of the Creative Commons CC BY-NC license, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited. You may not use the material for commercial purposes. |
spellingShingle | Review Kusuma, Gina D. Georgiou, Harry M. Perkins, Anthony V. Abumaree, Mohamed H. Brennecke, Shaun P. Kalionis, Bill Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress Associated with Preeclampsia |
title | Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress
Associated with Preeclampsia |
title_full | Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress
Associated with Preeclampsia |
title_fullStr | Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress
Associated with Preeclampsia |
title_full_unstemmed | Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress
Associated with Preeclampsia |
title_short | Mesenchymal Stem/Stromal Cells and Their Role in Oxidative Stress
Associated with Preeclampsia |
title_sort | mesenchymal stem/stromal cells and their role in oxidative stress
associated with preeclampsia |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8961706/ https://www.ncbi.nlm.nih.gov/pubmed/35370491 |
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