Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia

Johansen, Marianne; Redman, Christopher W.G.; Wilkins, T; Sargent, Ian L.

doi:10.1053/plac.1999.0422

Cited by 208 publications

(114 citation statements)

References 24 publications

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“…In normal pregnancy, trophoblast cells and syncytiotrophoblast microparticles are spontaneously shed from the placenta into the maternal circulation as part of the of normal placental physiologic turnover. [38][39][40] Syncytiotrophoblast membrane microparticles have previously been prepared in vitro from term placental villous explant cultures. 41 Furthermore there is evidence that microparticulate material can affect endothelial integrity.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

Oxygen and the liberation of placental factors responsible for vascular compromise

Robinson

Wareing

Hudson

et al. 2008

Laboratory Investigation

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“…Specifically, deportation of villous trophoblast debris directly into the maternal circulation [10][11][12]15 has been implicated in the genesis of the exaggerated intravascular maternal inflammatory response noted in patients with pre-eclampsia 13,14,[16][17][18] . However, whether trophoblast debris is generated through apoptosis or necrosis has not been determined [57][58][59] .…”

Section: Discussionmentioning

confidence: 99%

“…The placenta, but not the fetus, is required for the development of the disorder, as patients with classic 'hydatidiform moles' (without a fetus) can develop pre-eclampsia 2 . The mechanisms responsible for the genesis of the syndrome are poorly understood 3,4 , although roles for uteroplacental ischemia [5][6][7][8] , endothelial cell dysfunction 9 and exaggerated maternal inflammatory response to deported trophoblast have been proposed [10][11][12][13][14][15][16][17][18] .…”

Section: Introductionmentioning

confidence: 99%

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Neale

Demasio

Illuzi

et al. 2003

The Journal of Maternal-Fetal & Neonatal Medicine

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“…Placental growth involves proliferation, differentiation and syncytial fusion of cytotrophoblasts, which is associated with significant release (grams per day) of microvesicles-encapsulated, cffDNA-containing apoptotic trophoblasts content into maternal circulation (Nelson 1996, Huppertz et al 1998, Huppertz & Kingdom 2004, Bischoff et al 2005, Taglauer et al 2014. These microparticles, also referred to as syncytiotrophoblast microvesicles (SCTMs), were first described more than 100 years ago in lung capillaries of women who died from preeclampsia (Schmorl 1893) and were later described as a feature of normal pregnancy, although increased in preeclampsia (Johansen et al 1999). SCTMs as well as cffDNA alone are pro-inflammatory , Redman & Sargent 2000, Phillippe 2015.…”

Section: Cell-free Dnamentioning

confidence: 99%

“…Along these lines, a major feature of the pathophysiology of PE is the failure of fetal trophoblasts to invade uterine arteries, resulting in reduced placental perfusion and ensued hypoxia/ ischemia. This localized oxygen and nutrient deprivation is associated with exaggerated trophoblast cell death (Jones & Fox 1980, Chua et al 1991, Knight et al 1998, Johansen et al 1999, Leung et al 2001, which has been suggested to directly contribute to the disease by releasing mediators of inflammation that promote endothelial activation and systemic maternal inflammation (Smarason et al 1993, Knight et al 1998, Redman & Sargent 2003. Although the etiology of PE is mostly unknown, a major hallmark is a generalized inflammatory response characterized by high cytokine levels, such as IL-1β, IL-6, IL-8 and tumor necrosis factor-α (Vince et al 1995, Mellembakken et al 2001, Laresgoiti-Servitje 2013, Harmon et al 2016.…”

Section: Preeclampsiamentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

213

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia

Cited by 208 publications

References 24 publications

Oxygen and the liberation of placental factors responsible for vascular compromise

Oxygen and the liberation of placental factors responsible for vascular compromise

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Sterile inflammation and pregnancy complications: a review

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