Small extracellular vesicles from plasma of women with preeclampsia increase myogenic tone and decrease endothelium-dependent relaxation of mouse mesenteric arteries

Powell, Juliana S.; Gandley, Robin E.; Lackner, Emily; Dolinish, Andrea; Ouyang, Yi‐Bing; Powers, Robert W.; Morelli, Adrián E.; Hubel, Carl A.; Sadovsky, Yoel

doi:10.1016/j.preghy.2022.02.005

Cited by 6 publications

(6 citation statements)

References 66 publications

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“…Recently, Powell et al, demonstrated that EVs from preeclamptic women contribute to arterial tone regulation. They documented that ex vivo exposure of isolated mouse mesenteric arteries to EVs purified from the plasma of pregnant women with preeclampsia led to constriction in response to intraluminal pressure and resistance to methacholine-stimulated relaxation [ 71 ]. Furthermore, it is also suggested that EVs-exosomes from preeclampsia contribute to the dissemination of endothelial damage by sequestering the free vascular endothelial growth factor (VEGF) in the maternal circulation [ 72 , 73 , 74 , 75 , 76 , 77 , 78 ].…”

Section: Preeclampsiamentioning

confidence: 99%

Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Sławek-Szmyt

Kawka-Paciorkowska

Ciepłucha

et al. 2022

JCM

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Cardiovascular diseases (CVDs) remain the leading cause of death in women worldwide. Although traditional risk factors increase later-life CVD, pregnancy-associated complications additionally influence future CVD risk in women. Adverse pregnancy outcomes, including preeclampsia and fetal growth restriction (FGR), are interrelated disorders caused by placental dysfunction, maternal cardiovascular maladaptation to pregnancy, and maternal abnormalities such as endothelial dysfunction, inflammation, hypercoagulability, and vasospasm. The pathophysiologic pathways of some pregnancy complications and CVDs might be linked. This review aimed to highlight the associations between specific adverse pregnancy outcomes and future CVD and emphasize the importance of considering pregnancy history in assessing a woman’s CVD risk. Moreover, we wanted to underline the role of maternal cardiovascular maladaptation in the development of specific pregnancy complications such as FGR.

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Section: Preeclampsiamentioning

confidence: 99%

Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Sławek-Szmyt

Kawka-Paciorkowska

Ciepłucha

et al. 2022

JCM

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“…Similarly, Han et al (2020) found EVs from freeze-thaw-injured placenta induced hypertension and proteinuria when administered to non-pregnant mice, disrupted endothelial integrity and induced vasoconstriction. Powell et al (2022) demonstrated the uptake of sEVs from human maternal plasma into the vessel wall of mouse mesenteric arteries. Exposure to sEVs isolated from the plasma of individuals with PE produced significantly more vasoconstriction and less endothelium-induced relaxation in these vessels than sEVs from plasma of individuals without PE.…”

Section: Extracellular Vesicles In Obstetric Diseasesmentioning

confidence: 98%

“…Powell et al. (2022) demonstrated the uptake of sEVs from human maternal plasma into the vessel wall of mouse mesenteric arteries. Exposure to sEVs isolated from the plasma of individuals with PE produced significantly more vasoconstriction and less endothelium‐induced relaxation in these vessels than sEVs from plasma of individuals without PE.…”

Section: Introductionmentioning

confidence: 99%

Extracellular vesicles as markers and mediators of pregnancy complications: gestational diabetes, pre‐eclampsia, preterm birth and fetal growth restriction

Farrelly

Kennedy

Spencer

et al. 2023

The Journal of Physiology

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In high income countries, approximately 10% of pregnancies are complicated by pre‐eclampsia (PE), preterm birth (PTB), fetal growth restriction (FGR) and/or macrosomia resulting from gestational diabetes (GDM). Despite the burden of disease this places on pregnant people and their newborns, there are still few, if any, effective ways of preventing or treating these conditions. There are also gaps in our understanding of the underlying pathophysiologies and our ability to predict which mothers will be affected. The placenta plays a crucial role in pregnancy, and alterations in placental structure and function have been implicated in all of these conditions. As extracellular vesicles (EVs) have emerged as important molecules in cell‐to‐cell communication in health and disease, recent research involving maternal‐ and placental‐derived EV has demonstrated their potential as predictive and diagnostic biomarkers of obstetric disorders. This review will consider how placental and maternal EVs have been investigated in pregnancies complicated by PE, PTB, FGR and GDM and aims to highlight areas where further research is required to enhance the management and eventual treatment of these pathologies. image

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“…So, there could be bidirectional trafficking of inflammatory human EVs (and possibly BEVs) between the mother and fetus [29,30,230] . This is a precursor for inflammation-associated placental dysfunction, preeclampsia, fetal growth restriction, spontaneous preterm labor and postnatal developmental impairments [35,230,[311][312][313][314] .…”

Section: Stimulation Of Preeclampsia Preterm Labor and Birthmentioning

confidence: 99%

Cargo exchange between human and bacterial extracellular vesicles in gestational tissues: a new paradigm in communication and immune development

Amabebe,

Kumar,

Tatiparthy

et al. 2024

Extracell Vesicles Circ Nucleic Acids

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Host-bacteria and bacteria-bacteria interactions can be facilitated by extracellular vesicles (EVs) secreted by both human and bacterial cells. Human and bacterial EVs (BEVs) propagate and transfer immunogenic cargos that may elicit immune responses in nearby or distant recipient cells/tissues. Hence, direct colonization of tissues by bacterial cells is not required for immunogenic stimulation. This phenomenon is important in the feto-maternal interface, where optimum tolerance between the mother and fetus is required for a successful pregnancy. Though the intrauterine cavity is widely considered sterile, BEVs from diverse sources have been identified in the placenta and amniotic cavity. These BEVs can be internalized by human cells, which may help them evade host immune surveillance. Though it appears logical, whether bacterial cells internalize human EVs or human EV cargo is yet to be determined. However, the presence of BEVs in placental tissues or amniotic cavity is believed to trigger a low-grade immune response that primes the fetal immune system for ex-utero survival, but is insufficient to disrupt the progression of pregnancy or cause immune intolerance required for adverse pregnancy events. Nevertheless, the exchange of bioactive cargos between human and BEVs, and the mechanical underpinnings and health implications of such interactions, especially during pregnancy, are still understudied. Therefore, while focusing on the feto-maternal interface, we discussed how human cells take up BEVs and whether bacterial cells take up human EVs or their cargo, the exchange of cargos between human and BEVs, host cell (feto-maternal) inflammatory responses to BEV immunogenic stimulation, and associations of these interactions with fetal immune priming and adverse reproductive outcomes such as preeclampsia and preterm birth.

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Small extracellular vesicles from plasma of women with preeclampsia increase myogenic tone and decrease endothelium-dependent relaxation of mouse mesenteric arteries

Cited by 6 publications

References 66 publications

Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Extracellular vesicles as markers and mediators of pregnancy complications: gestational diabetes, pre‐eclampsia, preterm birth and fetal growth restriction

Cargo exchange between human and bacterial extracellular vesicles in gestational tissues: a new paradigm in communication and immune development

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