Foetoplacental communication via extracellular vesicles in normal pregnancy and preeclampsia

Chiarello, Delia I.; Salsoso, Rocío; Toledo, Fernando; Mate, Alfonso; Vázquez, Carmen M.; Sobrevía, Luis

doi:10.1016/j.mam.2017.12.002

Cited by 66 publications

(57 citation statements)

References 136 publications

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“…Endoglin-containing EVs are also increased in pre-eclampsia [84]. Finally, galectin-13, a key regulator of immune homeostasis by inducing T cell death and inflammation, has been shown to be increased in the cargo of EVs from preeclamptic pregnancies [77]. Finally, galectin-13, a key regulator of immune homeostasis by inducing T cell death and inflammation, has been shown to be increased in the cargo of EVs from preeclamptic pregnancies [77].…”

Section: Effects Of Placental Evs From Pre-eclamptic Pregnancies On Tmentioning

confidence: 99%

“…The involvement of EVs in the aetiology of pre-eclamptic pregnancies has been supposed based on both qualitative as well as quantitative molecular differences in placental EVs observed in pre-eclampsia [77]. Compared to normal first-term placentae, placental EVs from preeclamptic women tend to exacerbate the maternal immune response to LPS, which is normally reduced during gestation [78].…”

Section: Effects Of Placental Evs From Pre-eclamptic Pregnancies On Tmentioning

confidence: 99%

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Embryonic extracellular vesicles as informers to the immune cells at the maternal–fetal interface

Giacomini

Alleva

Fornelli

et al. 2019

Clinical and Experimental Immunology

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Extracellular vesicle (EV) exchange is emerging as a novel method of communication at the maternal-fetal interface. The presence of the EVs has been demonstrated in the preimplantation embryo culture medium from different species, such as bovines, porcines and humans. Preimplantation embryo-derived EVs have been shown to carry molecules potentially able to modulate the local endometrial immune system. The non-classical major histocompatibility complex (MHC) class I molecule human leucocyte antigen (HLA)-G, the immunomodulatory molecule progesterone-induced blocking factor and some regulatory miRNAs species are contained in embryo-derived EV cargo. The implanted syncytiotrophoblasts are also well known to secrete EVs, with microvesicles exerting a mainly proinflammatory effect while exosomes in general mediate local immunotolerance. This review focuses on the current knowledge on the potential role of EVs released by the embryo in the first weeks of pregnancy on the maternal immune cells. Collectively, the data warrant further exploration of the dialogue between the mother and the embryo via EVs.

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Section: Effects Of Placental Evs From Pre-eclamptic Pregnancies On Tmentioning

confidence: 99%

Section: Effects Of Placental Evs From Pre-eclamptic Pregnancies On Tmentioning

confidence: 99%

Embryonic extracellular vesicles as informers to the immune cells at the maternal–fetal interface

Giacomini

Alleva

Fornelli

et al. 2019

Clinical and Experimental Immunology

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“…; Chiarello et al . ). The placenta of preeclamptic women is characterized by shallow trophoblast invasion and unconverted narrow spiral arteries (Goldman‐Wohl & Yagel, ).…”

Section: Introductionmentioning

confidence: 97%

“…Although in recent decades much effort had been put in, preeclampsia-related complications remain a major cause for morbidity and mortality in pregnant women and fetuses (Duley, 2009). The mechanism that underlies the pathogenesis of preeclampsia is not completely understood, but this disorder is thought to be due to insufficient trophoblast invasion and placental dysfunction (Fisher, 2015;Chiarello et al 2018). Failure of proper trophoblast migration and invasion into decidua and uterine spiral arteries results in deficient remodelling and transformation from highto low-resistance vessels, leading to a sustained hypoxic environment and implicating the development of preeclampsia (Nakashima et al 2017;Chiarello et al 2018).…”

Section: Introductionmentioning

confidence: 99%

“…The mechanism that underlies the pathogenesis of preeclampsia is not completely understood, but this disorder is thought to be due to insufficient trophoblast invasion and placental dysfunction (Fisher, 2015;Chiarello et al 2018). Failure of proper trophoblast migration and invasion into decidua and uterine spiral arteries results in deficient remodelling and transformation from highto low-resistance vessels, leading to a sustained hypoxic environment and implicating the development of preeclampsia (Nakashima et al 2017;Chiarello et al 2018). The placenta of preeclamptic women is characterized by shallow trophoblast invasion and unconverted narrow spiral arteries (Goldman-Wohl & Yagel, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Elevated miR‐200a and miR‐141 inhibit endocrine gland‐derived vascular endothelial growth factor expression and ciliogenesis in preeclampsia

Wang

Tsai

Chen

et al. 2019

The Journal of Physiology

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Key points Endocrine gland‐derived vascular endothelial growth factor (EG‐VEGF) is a critical factor that facilitates trophoblast invasion in placenta. Plasma miR‐141 and miR‐200a levels were elevated, while EG‐VEGF was decreased in peripheral blood and placenta of preeclamptic patients. Furthermore, numbers of cilia in the placenta from preeclamptic women were significantly decreased. Elevated miR‐141 and miR‐200a inhibited the expression of EG‐VEGF, downstream extracellular signal‐regulated kinase (ERK)/matrix metalloproteinase 9 signalling and cilia formation, thus leading to defective trophoblast invasion. The growth of the primary cilium, which transduced ERK signalling upon EG‐VEGF induction for proper trophoblast invasion, was also inhibited by miR‐141 and miR‐200a upregulation. Abstract Preeclampsia is a severe gestational complication, and inadequate trophoblast invasion during placental development is an important pathoaetiology. Endocrine gland‐derived vascular endothelial growth factor (EG‐VEGF) is a critical factor that facilitates trophoblast invasion in placenta. By binding to the primary cilium, EG‐VEGF initiates the signalling cascade for proper embryo implantation and placental development. The miR‐200 family was predicted to target the EG‐VEGF 5′‐untranslated region, and its specific binding site was confirmed using a dual luciferase and a co‐transfection assay. In the peripheral blood and placenta of preeclamptic patients, EG‐VEGF showed significantly lower expression, whereas plasma miR‐141 and miR‐200a had higher expression compared with the controls. The biological significance of miR‐141 and miR‐200a was verified using an overexpression method in a trophoblast cell line (HTR‐8/SVneo). Elevated miR‐141 and miR‐200a inhibited the expression of EG‐VEGF, matrix metalloproteinase 9 (MMP9) and downstream extracellular signal‐regulated kinase (ERK) signalling, thus leading to defective trophoblast invasion. Additionally, the growth of the primary cilium, which transduces ERK/MMP9 signalling upon EG‐VEGF induction, was inhibited by miR‐141 and miR‐200a upregulation. Furthermore, the number of cilia in the human placenta of preeclamptic women was significantly decreased compared to normal placenta. In conclusion, the study uncovers the clinical correlations among the miR‐200 family, EG‐VEGF and the primary cilium in preeclampsia and the underlying molecular mechanisms. The results indicate that miR‐141 and miR‐200a directly targeted EG‐VEGF, suppressed primary cilia formation and inhibited trophoblast invasion. Thus, miR‐141 and miR‐200a could be explored as promising miRNA biomarkers and therapeutic targets in preeclampsia.

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Circulating Non-coding RNAs and Exosomes: Liquid Biopsies for Monitoring Preeclampsia

Ying

Tang

et al. 2023

Methods in Molecular Biology

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Foetoplacental communication via extracellular vesicles in normal pregnancy and preeclampsia

Cited by 66 publications

References 136 publications

Embryonic extracellular vesicles as informers to the immune cells at the maternal–fetal interface

Embryonic extracellular vesicles as informers to the immune cells at the maternal–fetal interface

Elevated miR‐200a and miR‐141 inhibit endocrine gland‐derived vascular endothelial growth factor expression and ciliogenesis in preeclampsia

Circulating Non-coding RNAs and Exosomes: Liquid Biopsies for Monitoring Preeclampsia

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