Placental extracellular vesicles and pre‐eclampsia

Pre‐eclampsia is a hypertensive disease of pregnancy characterized by new‐onset hypertension, with either proteinuria and/or organ dysfunction. Pre‐eclampsia is a leading cause of maternal morbidity and mortality; however, the underlying cellular and molecular mechanisms are not well understood. The...

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Published inAmerican journal of reproductive immunology (1989) Vol. 85; no. 2; pp. e13297 - n/a
Main Authors Schuster, Jessica, Cheng, Shi‐Bin, Padbury, James, Sharma, Surendra
Format Journal Article
LanguageEnglish
Published Denmark Wiley Subscription Services, Inc 01.02.2021
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Abstract Pre‐eclampsia is a hypertensive disease of pregnancy characterized by new‐onset hypertension, with either proteinuria and/or organ dysfunction. Pre‐eclampsia is a leading cause of maternal morbidity and mortality; however, the underlying cellular and molecular mechanisms are not well understood. There is consensus that the underlying mechanism(s) resulting in pre‐eclampsia is centered around abnormal placentation, inadequate spiral‐artery remodeling, and deficiency in trophoblast invasion, resulting in impaired maternal blood flow to the placenta and a release of signals and/or inflammatory mediators into maternal circulation triggering the systemic manifestations of pre‐eclampsia. ER stress, resulting in impaired autophagy and placental release of aggregated proteins, may also confer systemic stress to maternal organs in pre‐eclampsia. Extracellular vesicles (EVs), lipid‐bilayer enclosed structures containing macromolecules including proteins, miRNA, and other important nucleotides, have been suggested to play an important role in this maternal‐fetal communication. Circulating EVs are present in greater quantity in the plasma of pre‐eclampsia subjects compared to normal pregnancy, and the placental derived EVs have been shown to have altered protein and RNA cargo. In this review, we will focus on EVs and their role in pre‐eclampsia, specifically their role in immune responses, inflammation, altered angiogenesis, and endothelial dysfunction.
AbstractList Pre‐eclampsia is a hypertensive disease of pregnancy characterized by new‐onset hypertension, with either proteinuria and/or organ dysfunction. Pre‐eclampsia is a leading cause of maternal morbidity and mortality; however, the underlying cellular and molecular mechanisms are not well understood. There is consensus that the underlying mechanism(s) resulting in pre‐eclampsia is centered around abnormal placentation, inadequate spiral‐artery remodeling, and deficiency in trophoblast invasion, resulting in impaired maternal blood flow to the placenta and a release of signals and/or inflammatory mediators into maternal circulation triggering the systemic manifestations of pre‐eclampsia. ER stress, resulting in impaired autophagy and placental release of aggregated proteins, may also confer systemic stress to maternal organs in pre‐eclampsia. Extracellular vesicles (EVs), lipid‐bilayer enclosed structures containing macromolecules including proteins, miRNA, and other important nucleotides, have been suggested to play an important role in this maternal‐fetal communication. Circulating EVs are present in greater quantity in the plasma of pre‐eclampsia subjects compared to normal pregnancy, and the placental derived EVs have been shown to have altered protein and RNA cargo. In this review, we will focus on EVs and their role in pre‐eclampsia, specifically their role in immune responses, inflammation, altered angiogenesis, and endothelial dysfunction.
Pre-eclampsia is a hypertensive disease of pregnancy characterized by new-onset hypertension, with either proteinuria and/or organ dysfunction. Pre-eclampsia is a leading cause of maternal morbidity and mortality; however, the underlying cellular and molecular mechanisms are not well understood. There is consensus that the underlying mechanism(s) resulting in pre-eclampsia is centered around abnormal placentation, inadequate spiral-artery remodeling, and deficiency in trophoblast invasion, resulting in impaired maternal blood flow to the placenta and a release of signals and/or inflammatory mediators into maternal circulation triggering the systemic manifestations of pre-eclampsia. ER stress, resulting in impaired autophagy and placental release of aggregated proteins, may also confer systemic stress to maternal organs in pre-eclampsia. Extracellular vesicles (EVs), lipid-bilayer enclosed structures containing macromolecules including proteins, miRNA, and other important nucleotides, have been suggested to play an important role in this maternal-fetal communication. Circulating EVs are present in greater quantity in the plasma of pre-eclampsia subjects compared to normal pregnancy, and the placental derived EVs have been shown to have altered protein and RNA cargo. In this review, we will focus on EVs and their role in pre-eclampsia, specifically their role in immune responses, inflammation, altered angiogenesis, and endothelial dysfunction.Pre-eclampsia is a hypertensive disease of pregnancy characterized by new-onset hypertension, with either proteinuria and/or organ dysfunction. Pre-eclampsia is a leading cause of maternal morbidity and mortality; however, the underlying cellular and molecular mechanisms are not well understood. There is consensus that the underlying mechanism(s) resulting in pre-eclampsia is centered around abnormal placentation, inadequate spiral-artery remodeling, and deficiency in trophoblast invasion, resulting in impaired maternal blood flow to the placenta and a release of signals and/or inflammatory mediators into maternal circulation triggering the systemic manifestations of pre-eclampsia. ER stress, resulting in impaired autophagy and placental release of aggregated proteins, may also confer systemic stress to maternal organs in pre-eclampsia. Extracellular vesicles (EVs), lipid-bilayer enclosed structures containing macromolecules including proteins, miRNA, and other important nucleotides, have been suggested to play an important role in this maternal-fetal communication. Circulating EVs are present in greater quantity in the plasma of pre-eclampsia subjects compared to normal pregnancy, and the placental derived EVs have been shown to have altered protein and RNA cargo. In this review, we will focus on EVs and their role in pre-eclampsia, specifically their role in immune responses, inflammation, altered angiogenesis, and endothelial dysfunction.
Author Padbury, James
Cheng, Shi‐Bin
Schuster, Jessica
Sharma, Surendra
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Issue 2
Keywords placenta
pre-eclampsia
extracellular vesicles
Language English
License 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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Notes Funding information
This work was supported in part by the NIH P20 GM121298 and P30 GM114750 grants.
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Snippet Pre‐eclampsia is a hypertensive disease of pregnancy characterized by new‐onset hypertension, with either proteinuria and/or organ dysfunction. Pre‐eclampsia...
Pre-eclampsia is a hypertensive disease of pregnancy characterized by new-onset hypertension, with either proteinuria and/or organ dysfunction. Pre-eclampsia...
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SubjectTerms Angiogenesis
Animals
Autophagy
Blood flow
Eclampsia
Extracellular vesicles
Extracellular Vesicles - metabolism
Female
Fetuses
Humans
Immune response
Immunity - immunology
Inflammation
Inflammation - immunology
Macromolecules
miRNA
Molecular modelling
Morbidity
Neovascularization, Pathologic
Nucleotides
Phagocytosis
Placenta
Placenta - metabolism
Pre-Eclampsia - immunology
Preeclampsia
Pregnancy
pre‐eclampsia
Proteinuria
Title Placental extracellular vesicles and pre‐eclampsia
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Faji.13297
https://www.ncbi.nlm.nih.gov/pubmed/32619308
https://www.proquest.com/docview/2488494274
https://www.proquest.com/docview/2420144594
Volume 85
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