Purification and Characterization of a Complex from Placental Syncytiotrophoblast Microvillous Membranes which Inhibits the Proliferation of Human Umbilical Vein Endothelial Cells

Kertész, Zsuzsa; Hurst, Georgina; Ward, Monika A.; Willis, Anthony C.; Caro, H; Linton, E.A.; Sargent, Ian L.; Redman, Christopher W.G.

doi:10.1053/plac.1998.0351

Cited by 27 publications

(18 citation statements)

References 34 publications

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“…41 Furthermore there is evidence that microparticulate material can affect endothelial integrity. 42 In the present study, following the removal of particulate material, exposure to hypoxic explant medium still resulted in both an increase in cell death, as evidenced by mitochondrial depolarization, and reduced endothelial cellular ATP levels. Thus, it appears that placental factor(s) other than shed microparticles can affect endothelial cell metabolism.…”

Section: Discussionmentioning

confidence: 42%

Oxygen and the liberation of placental factors responsible for vascular compromise

Robinson

Wareing

Hudson

et al. 2008

Laboratory Investigation

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Maternal endothelial activation in pre-eclampsia is attributed to the release of unknown factors from a hypoperfused placenta. To further characterize these factors, we have used a serum-free placental villous explant culture model and investigated the effect of the liberated soluble factors produced on human endothelial cell cultures. Term placental villous explants from uncomplicated pregnancies were cultured for 4 days in 20, 6 or 1% O 2 to mimic placental hyperoxia, normoxia and hypoxia. Medium collected from viable explants was applied to cultured human uterine microvascular endothelial cells. Medium conditioned by hypoxic explants caused a significant decrease in endothelial cell ATP levels and mitochondrial dehydrogenase activity, suggestive of a reduced metabolic rate. An additional reduction in mitochondrial membrane potential and increased endothelial cell death occurred as the oxygen concentration to which explants had been exposed decreased. Effects of the hypoxic explant medium were also seen ex vivo in a wire myography model of myometrial artery function, with increased vasoconstriction and attenuated vasodilation following exposure to hypoxic explant medium. These results suggest that hypoxia (1% O 2 ) may stimulate the release of soluble factors from the placenta, which have an adverse effect on endothelial cell metabolism and mitochondrial integrity in vitro. These potentially pathogenic factors are now being characterized.

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Section: Discussionmentioning

confidence: 42%

Oxygen and the liberation of placental factors responsible for vascular compromise

Robinson

Wareing

Hudson

et al. 2008

Laboratory Investigation

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“…Salomon et al (2013a) identified fms-related tyrosine kinase 1 (FLT1, also known as vascular endothelial growth factor receptor 1, VEGFR1). Intriguingly, CD81, CD63, ICAM-1 and PLAP were used to select sucrose-gradient fractions positive for trophoblast-derived exosomes (Atay et al 2011;Salomon et al 2013a) and other studies have reported that STBEVs contain these proteins (Kertesz et al 1999;Guller et al 2011;Tannetta et al 2013), so it is puzzling why some of these marker proteins were not listed as identified proteins in the proteomic analyses.…”

Section: Proteinsmentioning

confidence: 99%

Placenta-derived extracellular vesicles: their cargo and possible functions

Familari

Cronqvist

Masoumi

et al. 2017

Reprod. Fertil. Dev.

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The literature on extracellular vesicles consists of rapidly expanding and often contradictory information. In this paper we attempt to review what is currently known regarding extracellular vesicles released specifically from human placental syncytiotrophoblast cells with a focus on the common but complex pregnancy-associated syndrome pre-eclampsia, where the level of syncytiotrophoblast extracellular vesicle release is significantly increased. We review common methods for syncytiotrophoblast extracellular vesicle derivation and isolation and we discuss the cargo of syncytiotrophoblast extracellular vesicles including proteins, RNA and lipids and their possible functions. A meta-analysis of available trophoblast-derived extracellular vesicle proteomic datasets revealed only three proteins in common: albumin, fibronectin-1 and plasminogen activator inhibitor-1, suggesting some variability in vesicle cargo, most likely reflecting stage and cell type of origin. We discuss the possible sources of variability that may have led to the low number of common markers, which has led us to speculate that markers and density in common use may not be strict criteria for identifying and isolating placenta-derived exosomes.

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“…1j); at the same time, the Nv and Sv of the syncytiotrophoblast microvilli were significantly lower than in normal placentas (Fig. 1g-m), which suggested increased STBM shedding in PE placentas (Germain et al 2007;Kertesz et al 1999;Redman and Sargent 2000). The actin cytoskeleton is essential for the adherence and fusion of the trophoblast (Shibukawa et al 2010) and has attracted special attention in placenta-related diseases (Miehe et al 2006).…”

Section: Discussionmentioning

confidence: 91%

RhoB/ROCK mediates oxygen–glucose deprivation-stimulated syncytiotrophoblast microparticle shedding in preeclampsia

Han

Yang

et al. 2016

Cell Tissue Res

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Increased circulating syncytiotrophoblast microparticles (STBMs) are often associated with preeclampsia (PE) but the molecular mechanisms regulating STBM shedding remain elusive. Experimental evidence has shown that actin plays a key role in STBM shedding and that Rho/ROCK is important in regulating actin rearrangement. To investigate the role of RhoB/ROCK-regulated actin arrangement in STBM shedding in PE, chorionic villous explants were prepared from placenta of patients with normotensive or PE pregnancies and BeWo cells were fused to imitate syncytiotrophoblasts. The oxygen-glucose deprivation (OGD) conditions were applied to imitate the pathophysiology of PE in vitro. The results showed that RhoB and ROCK were activated in the preeclamptic placenta, accompanied by increased actin polymerization and decreased outgrowing microvilli. In villous tissue cultures or BeWo cells, OGD activated RhoB, ROCK1 and ROCK2 and promoted STBM shedding and actin stress fibers formation. In BeWo cells, RhoB overexpression activated ROCK1 and ROCK2, leading to F-actin redistribution and STBM shedding and the OGD-induced actin polymerization and STBM shedding could be reversed by RhoB or ROCK knockdown. These results reveal that RhoB and ROCK play a key role in PE by targeting STBM shedding through actin rearrangement and that RhoB/ROCK intervention may be a potential therapeutic strategy for PE.

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Purification and Characterization of a Complex from Placental Syncytiotrophoblast Microvillous Membranes which Inhibits the Proliferation of Human Umbilical Vein Endothelial Cells

Cited by 27 publications

References 34 publications

Oxygen and the liberation of placental factors responsible for vascular compromise

Oxygen and the liberation of placental factors responsible for vascular compromise

Placenta-derived extracellular vesicles: their cargo and possible functions

RhoB/ROCK mediates oxygen–glucose deprivation-stimulated syncytiotrophoblast microparticle shedding in preeclampsia

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