Lipidomic analysis of human placental Syncytiotrophoblast microvesicles in adverse pregnancy outcomes

Baig, Sonia; Lim, Ju Young; Fernandis, Aaron Z.; Wenk, Markus R.; Kale, Anita Sugam; Su, Lin; Biswas, Arijit; Vasoo, S; Shui, Guanghou; Choolani, Mahesh

doi:10.1016/j.placenta.2013.02.004

Cited by 113 publications

(109 citation statements)

References 45 publications

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“…45 Proteomic and lipidomic contents of microvesicles generated by syncytiotrophoblasts have also been investigated in normal and complicated pregnancies. 28,59 Microvesicles in these reports ranged from 30 nm-1 mm in size. Of the w200 lipids reported, higher levels of phosphatidylserine and lower phosphatidic acid, phosphatidylglycerol, and ganglioside mannoside 3 were reported in pregnancies complicated with preeclampsia and recurrent miscarriage compared to controls.…”

Section: Ajogorgmentioning

confidence: 94%

Placental exosomes in normal and complicated pregnancy

Mitchell

Peiris

Kobayashi

et al. 2015

American Journal of Obstetrics and Gynecology

312

316

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Section: Ajogorgmentioning

confidence: 94%

Placental exosomes in normal and complicated pregnancy

Mitchell

Peiris

Kobayashi

et al. 2015

American Journal of Obstetrics and Gynecology

312

316

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“…It has been shown that exosomes, in general, are enriched for cholesterol and sphingomyelins, which may modulate recipient cell homeostasis (Baig et al 2013;Record et al 2014). The levels of various lipids are altered in the placenta in preeclampsia, as well as recurrent miscarriage, and as exposed negatively charged lipids may stimulate thrombosis, the increased load of placental extracellular vesicles observed in preeclampsia may contribute to the pathogenesis of this condition (Alijotas-Reig et al 2009;Baig et al 2013).…”

Section: Lipidsmentioning

confidence: 99%

“…The levels of various lipids are altered in the placenta in preeclampsia, as well as recurrent miscarriage, and as exposed negatively charged lipids may stimulate thrombosis, the increased load of placental extracellular vesicles observed in preeclampsia may contribute to the pathogenesis of this condition (Alijotas-Reig et al 2009;Baig et al 2013). Interestingly, placental microvesicles produced by mechanical disruption of the placenta are reported to carry more lipids than microvesicles produced via perfusion or explant culture methods (Gupta et al 2008).…”

Section: Lipidsmentioning

confidence: 99%

Placental Extracellular Vesicles and Feto-Maternal Communication

Tong

Chamley

2015

Cold Spring Harbor Perspectives in Medicine

122

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The human placenta is an anatomically unique structure that extrudes a variety of extracellular vesicles into the maternal blood (including syncytial nuclear aggregates, microvesicles, and nanovesicles). Large quantities of extracellular vesicles are produced by the placenta in both healthy and diseased pregnancies. Since their first description more than 120 years ago, placental extracellular vesicles are only now being recognized as important carriers for proteins, lipids, and nucleic acids, which may play a crucial role in feto-maternal communication. Here, we summarize the current literature on the cargos of placental extracellular vesicles and the known effects of such vesicles on maternal cells/systems, especially those of the maternal immune and vascular systems.T he placenta is an unusual organ with a short and defined life span. The human placenta is a fetal organ that sits between the fetus and its mother, connecting the fetus to the maternal blood supply. It is highly invasive and the entire surface of the placenta is in contact with the maternal circulation during most of gestation. Therefore, the human placenta effectively behaves as one wall of a maternal "blood vessel." This phenomenon is quite remarkable because, being a fetal organ, the placenta is in essence a semiallogeneic tissue graft in normal pregnancy and a complete allograft in surrogate or donor egg pregnancies. Therefore, the placenta is nature's only tissue graft.The human placenta has a villous (branching) structure. The surface of placental villi is covered by the multinucleated syncytiotrophoblast that is terminally differentiated and is not mitotically active. The growth and replenishment of the syncytiotrophoblast is effected by fusion of underlying mononuclear cytotrophoblasts into this layer. Beneath the cytotrophoblasts is the mesenchymal core of the villus with fetal blood vessels. The syncytiotrophoblast is a remarkable cell, which at least in theory, is a single cell covering the entire surface of the placenta and is the immunological barrier between the maternal immune system and the fetus. In a normal term placenta, the syncytiotrophoblast has an area of some 11 -13 m 2 (Mayhew 2014). However, the syncytiotrophoblast can be denuded, leaving areas lined by fibrinoid rather than syncytiotrophoblast and presumably before the laying down of this fibrinoid, cells of the villous mesenchymal core or cytotrophoblasts are exposed to the maternal blood, at least temporarily.

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“…Our study suggested that down-regulation of NTE in preeclamptic women would result in up-regulation of membrane PC levels and down-regulation of choline in human placenta, which could be related to the toxicity trophoblast cells. Furthermore, epidemic studies showed that the levels of placental PC, PS and triglyceride were significantly increased in preeclamptic pregnancy compared to normal pregnancy [20, 26]. Kobayashi et al also reported that eclamptic seizures may be induced when patients with severe PE were administrated by an anticholinergic (scopolamine butylbromide), blocking the function of choline [27].…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of Neuropathy Target Esterase in Preeclampsia Placenta Inhibits Human Trophoblast Cell Invasion via Modulating MMP-9 Levels

Zhong

Chen

Ling

et al. 2018

Cell Physiol Biochem

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Background/Aims: Neuropathy target esterase (NTE, also known as neurotoxic esterase) is proven to deacylate phosphatidylcholine (PC) to glycerophosphocholine as a phospholipase B. Recently; studies showed that artificial phosphatidylserine/PC microvesicles can induce preeclampsia (PE)-like changes in pregnant mice. However, it is unclear whether NTE plays a key role in the pathology of PE, a pregnancy-related disease, which was characterized by deficient trophoblast invasion and reduced trophoblast-mediated remodeling of spiral arteries. The aim of this study was to investigate the expression pattern of NTE in the placenta from women with PE and normal pregnancy, and the molecular mechanism of NTE involved in the development of PE. Methods: NTE expression levels in placentas from 20 pregnant women with PE and 20 healthy pregnant women were detected using quantitative PCR and immunohistochemistry staining. The effect of NTE on trophoblast migration and invasion and the underlying mechanisms were examined in HTR-8/SVneo cell lines by transfection method. Results: NTE mRNA and protein expression levels were significantly decreased in preeclamptic placentas than normal control. Over-expression of NTE in HTR-8/SVneo cells significantly promoted trophoblast cells migration and invasion and was associated with increased MMP-9 levels. Conversely, shRNA-mediated down-regulation of NTE markedly inhibited the cell migration and invasion. In addition, silencing NTE reduced the MMP-9 activity and phosphorylated Erk1/2 and AKT levels. Conclusions: Our results suggest that the decreased NTE may contribute to the development of PE through impairing trophoblast invasion by down-regulating MMP-9 via the Erk1/2 and AKT signaling pathway.

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Lipidomic analysis of human placental Syncytiotrophoblast microvesicles in adverse pregnancy outcomes

Cited by 113 publications

References 45 publications

Placental exosomes in normal and complicated pregnancy

Placental exosomes in normal and complicated pregnancy

Placental Extracellular Vesicles and Feto-Maternal Communication

Down-Regulation of Neuropathy Target Esterase in Preeclampsia Placenta Inhibits Human Trophoblast Cell Invasion via Modulating MMP-9 Levels

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