Syncytiotrophoblast‐derived microparticle shedding in early‐onset and late‐onset severe pre‐eclampsia

Chen, Yu; Huang, Yajuan; Jiang, Ruming; Teng, Yincheng

doi:10.1016/j.ijgo.2012.07.010

Cited by 73 publications

(69 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is well documented that there is an increase in shedding of placental macrovesicles (SNAs) during preeclampsia (Attwood and Park 1961;Chua et al 1991;Buurma et al 2013). Similarly, the shedding of placental microvesicles into the maternal blood is also increased in women with early onset preeclampsia (Goswami et al 2006;Chen et al 2012b), with levels in the maternal blood correlating with systolic blood pressure (Lok et al 2008b). However, the level of circulating placental microvesicles does not seem to be altered in women with late onset preeclampsia or intrauterine growth restriction (Goswami et al 2006).…”

Section: The Production Of Placental Vesicles Is Increased In Preeclamentioning

confidence: 99%

“…von Dadelszen et al (1999) reported that the conditioned media derived from culturing endothelial cells with microvesicles from normal term placentae was proinflammatory and could activate resting monocytes, granulocytes, and lymphocytes (von Dadelszen et al 1999). It has also been shown that microvesicles derived from normal term placentae can inhibit proliferation and increase apoptosis of endothelial cells (Smarason et al 1993;Chen et al 2012b). Electron microscopic examination revealed extensive disruption of the usual honeycomb structure of the endothelium by placental microvesicles (Smarason et al 1993;Cockell et al 1997).…”

Section: Endothelial Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Placental Extracellular Vesicles and Feto-Maternal Communication

Tong

Chamley

2015

Cold Spring Harbor Perspectives in Medicine

123

View full text Add to dashboard Cite

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.

show abstract

Section: The Production Of Placental Vesicles Is Increased In Preeclamentioning

confidence: 99%

Section: Endothelial Cellsmentioning

confidence: 99%

Placental Extracellular Vesicles and Feto-Maternal Communication

Tong

Chamley

2015

Cold Spring Harbor Perspectives in Medicine

123

View full text Add to dashboard Cite

show abstract

“…6 The number of erythrocyte and endothelial MVs increases in severe PET, 7 and shedding of trophoblast MVs into maternal circulation is higher in early-onset than late-onset diseases. 8 It is of interest that MVs of women with PET were found to promote vascular wall inflammation. 9 Our previous study, characterizing MVs of normal healthy pregnant (NHP) women and women with gestational vascular complications (GVCs), including HT and PET, 10 showed that trophoblast MV levels were similar in these groups.…”

Section: Hypertensionmentioning

confidence: 99%

“…MV concentrations were measured using 7.5 µm count beads (Flow Cytometer Absolute Count Standard, Bangs Laboratories Inc., Indiana), as described previously. 8 . MVs were labeled with antibodies for 30 minutes, suspended in PBS containing 0.02% formaldehyde, and scanned by the CyAn ADP analyzer.…”

Section: Flow Cytometry Analysismentioning

confidence: 99%

Microvesicles of Women With Gestational Hypertension and Preeclampsia Affect Human Trophoblast Fate and Endothelial Function

et al. 2013

View full text Add to dashboard Cite

Microvesicles shedding from cell membrane affect inflammation, apoptosis, and angiogenesis. We hypothesize that microvesicles of women with gestational vascular complications reflect pathophysiological state of the patients and affect their endothelial and trophoblast cell function. Microvesicles of healthy pregnant women, women with gestational hypertension, mild, or severe preeclampsia/toxemia, were characterized, and their effects on early-stage or term trophoblasts and endothelial cells were evaluated using apoptosis, migration, and tube formation assays. Patient subgroups differed significantly only in proteinuria levels, therefore their microvesicles were assessed as 1 group, demonstrating higher levels of inflammatory and angiogenic proteins compared with those of healthy pregnant women. In endothelial cells, microvesicles of healthy pregnant women reduced caspase 3/7 activity, increased migration, and induced tube formation. These processes were suppressed by microvesicles of women with gestational vascular complications. In early-stage trophoblasts, microvesicles of healthy pregnant women decreased apoptosis compared with untreated cells (6±5% versus 13.8±5.8%; P <0.001) and caspase 3/7 activity and induced higher migration (39.7±10.1 versus 20.3±8.3 mm 2 ; P <0.001). This effect was mediated through extracellular signal-regulated kinase pathway. Conversely, microvesicles of women with gestational vascular complications increased term trophoblast apoptosis compared with cells exposed to microvesicles of healthy pregnant women (15.1±3.3% versus 6.5±2.1%; P <0.001) and inhibited early-stage trophoblasts migration (21.4±18.5 versus 39.7±10.1 mm 2 ; P <0.001). In conclusion, microvesicle content and effects on endothelial and trophoblast cells vary according to the physiological/pathological state of a pregnant woman. Microvesicles seem to play a pivotal role in the course of pregnancy, which could potentially result in gestational vascular complications.

show abstract

“…Syncytiotrophoblast extracellular vesicles (STBM) are continuously shed and secreted from the placental syncytium into the maternal circulation in normal pregnancy. Significantly increased amounts of STBM have been discovered in PE [6], especially in early-onset PE [7,8]. STBM mainly comprise microparticles and exosomes, which vary in size, morphology and function.…”

Section: Introductionmentioning

confidence: 99%

Differential Proteomic Analysis of Syncytiotrophoblast Extracellular Vesicles from Early-Onset Severe Preeclampsia, using 8-Plex iTRAQ Labeling Coupled with 2D Nano LC-MS/MS

Han

Yang

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Aims: Previous studies have revealed that the increased shedding of syncytiotrophoblast extracellular vesicles (STBM) may lead to preeclampsia (PE). We aimed to identify the proteins carried by STBM and their potential pathological roles in early-onset severe PE. Methods: In this study, we performed a differential proteomic analysis of STBM from early-onset severe PE patients, using iTRAQ isobaric tags and 2D nano LC-MS/MS. STBM were generated by the in vitro explant culture method, and then verified by electron microscopy and western blot analysis. Results: A total of 18 533 unique peptides and 3 317 proteins were identified, 3 292 proteins were quantified. We identified 194 differentially expressed proteins in STBM from early-onset severe PE patients, 122 proteins were up-regulated and 72 proteins were down-regulated. Further bioinformatics analysis revealed that mitochondrion, transmembrane transport and transmembrane transporter activity were the most abundant categories in gene ontology (GO) annotation. Glycolysis/ gluconeogenesis, citrate cycle, fatty acid elongation, steroid hormone biosynthesis and oxidative phosphorylation were the five significantly represented pathways. Four differentially expressed proteins (siglec-6, calnexin, CD63 and S100-A8) related to inflammation, coagulation or immunoregulation were independently verified using western blot. Conclusions: The identification of key proteins carried by STBM may serve not only as a basis for better understanding and further exploring the etiology and pathogenesis of PE, but also as potential biomarkers and in providing targets for future therapy in PE, especially in early-onset severe PE(sPE).

show abstract

Syncytiotrophoblast‐derived microparticle shedding in early‐onset and late‐onset severe pre‐eclampsia

Abstract: Shedding of STBMs into the maternal circulation occurs in greater amounts in early-onset pre-eclampsia than in late-onset pre-eclampsia.

Cited by 73 publications

References 24 publications

Placental Extracellular Vesicles and Feto-Maternal Communication

Placental Extracellular Vesicles and Feto-Maternal Communication

Microvesicles of Women With Gestational Hypertension and Preeclampsia Affect Human Trophoblast Fate and Endothelial Function

Differential Proteomic Analysis of Syncytiotrophoblast Extracellular Vesicles from Early-Onset Severe Preeclampsia, using 8-Plex iTRAQ Labeling Coupled with 2D Nano LC-MS/MS

Contact Info

Product

Resources

About