IFPA Meeting 2010 Workshops Report II: Placental pathology; Trophoblast invasion; Fetal sex; Parasites and the placenta; Decidua and embryonic or fetal loss; Trophoblast differentiation and syncytialisation

doi:10.1016/j.placenta.2010.12.025

Placenta

Volume 32, Supplement 2, March 2011, Pages S90-S99

https://doi.org/10.1016/j.placenta.2010.12.025 Get rights and content

Abstract

Workshops are an important part of the IFPA annual meeting. At IFPA Meeting 2010 diverse topics were discussed in twelve themed workshops, six of which are summarized in this report. 1. The placental pathology workshop focused on clinical correlates of placenta accreta/percreta. 2. Mechanisms of regulation of trophoblast invasion and spiral artery remodeling were discussed in the trophoblast invasion workshop. 3. The fetal sex and intrauterine stress workshop explored recent work on placental sex differences and discussed them in the context of whether boys live dangerously in the womb.4. The workshop on parasites addressed inflammatory responses as a sign of interaction between placental tissue and parasites. 5. The decidua and embryonic/fetal loss workshop focused on key regulatory mediators in the decidua, embryo and fetus and how alterations in expression may contribute to different diseases and adverse conditions of pregnancy. 6. The trophoblast differentiation and syncytialisation workshop addressed the regulation of villous cytotrophoblast differentiation and how variations may lead to placental dysfunction and pregnancy complications.

Section snippets

Placental pathology and clinical correlates (accrete/percreta)

Chairs: Abdulluh Al-Khan, Carolyn Salafia

Speakers: Alexandre Borbely, Sally Collins, Gladys Ramos

Trophoblast invasion

Chairs: Charles Graham, Peeyush Lala

Speakers: Ivraym Barsoum, Georgina Cerchi, Tiziana Cotechini, Thierry Fournier, Paula Headley, Charles Graham, Geeta Godbole, Peeyush Lala, Ellen Menkhorst

Fetal sex and intrauterine stress: boys live dangerously in the womb

Chairs: Vicki Clifton, Rohan Lewis

Speakers: Luciana Lassance, Rohan Lewis, Richard Saffery, Colin Sibley, Owen Vaughan

Parasites, infections and the placenta

Chairs: Henning Schneider, Ulrike Kemmerling

Speakers: Ashley Davey, Ricardo Fretes, Thierry Fournier, Stefan R. Hansson, Ulrike Kemmerling, Cindy Morris, Demba Sarr, Henning Schneider

Decidua, embryonic and fetal development and loss

Chairs:Elisa Cebral, Alicia Jawerbaum

Speakers: Elisa Cebral, Vicki Clifton, Ana Franchi, Cristina Ibarra, Michael Soares, Stacy Zamudio

Trophoblast differentiation and syncytialization

Chairs: Yoshiki Kudo, Neal Rote

Speakers: Irving Aye, Jesica Flores-Martin, Takahiro Nobuzane, Neal Rote, Ambika Singh, Tharini Sivasubramaniyam

Conflict of interest

The authors have no conflict of interest.

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Cited by (25)

Downregulation of miR-29a/b/c in placenta accreta inhibits apoptosis of implantation site intermediate trophoblast cells by targeting MCL1
2016, Placenta
Citation Excerpt :
Placenta accreta is a generalized term describing implantation of an abnormal, firmly adherent placenta that exhibits some degree of invasion into the uterus [1]. In 2011, the International Federation of Placenta Associations (IFPA) declared that the rise in cesarean sections is to blame for the increased incidence of placenta accreta in recent years [2]. In Italy, the incidence of placenta accreta increased from 0.12% during the 1970s to 0.31% during the 2000s.
Placenta accreta is defined as abnormal adhesion of placental villi to the uterine myometrium. Although this condition has become more common as a result of the increasing rate of cesarean sections, the underlying causative mechanism(s) remain elusive. Because microRNA-29a/b/c (miR-29a/b/c) have been shown to play important roles in placental development, this study evaluated the roles of these microRNAs in placenta accreta.
Expression of miR-29a/b/c and myeloid cell leukemia-1 (MCL1) were quantified in patient tissues and HTR8/SVneo trophoblast cells using the real-time quantitative polymerase chain reaction. Western blotting was used to analyze expression of the MCL1 protein in HTR8/SVneo trophoblast cells with altered expression of miR-29a/b/c. To determine their role in apoptosis, miR-29a/b/c were overexpressed in HTR-8/SVneo cells, and levels of apoptosis were analyzed by flow cytometry. Luciferase activity assays were used to determine whether MCL1 is a target gene of miR-29a/b/c.
Expression of miR-29a/b/c was significantly lower in creta sites compared to noncreta sites (p = 0.018, 0.041, and 0.022, respectively), but expression of MCL1 was upregulated in creta sites (p = 0.039). MCL1 expression was significantly downregulated in HTR-8/SVneo cells overexpressing miR-29a/b/c (p = 0.002, 0.008, and 0.013, respectively). Luciferase activity assays revealed that miR-29a/b/c directly target the 3′ untranslated region of MCL1 in 293T cells. Over-expression of miR-29a/b/c induced apoptosis in the HTR-8/SVneo trophoblast cell line. Moreover, histopathological evaluation revealed that the number of implantation site intermediate trophoblast (ISIT) cells was increased in creta sites and that these cells were positive for MCL1.
Our results demonstrate that in placenta accreta, miR-29a/b/c inhibits apoptosis of ISIT cells by targeting MCL1. These findings provide new insights into the pathogenesis of placenta accreta.
Decreased placental and maternal serum TRAIL-R2 levels are associated with placenta accreta
2016, Placenta
Citation Excerpt :
Previous reports indicated that the most important risk factor for placenta accreta is placenta previa in the presence of an uterine scar, and the remaining risk factors reported are multiparity, maternal age, any prior uterine surgery or curettage, uterine irradiation, endometrial ablation, Asherman syndrome or other uterine anomalies [1]. When all these associated risk factors are considered, it is clear that the common feature is the disruption of the fetal–maternal interface by the alterations in the local microenvironment [2]. Because abnormal placental invasion is commonly located in the area of the previous hysterotomy, and because the incidence of placenta accreta appears to be increasing parallel to the increasing number of cesarean deliveries, the scarring of the uterine wall, particularly by previous cesarean deliveries, is hypothesized as the most important risk factor leading to placental hyperinvasiveness [1,2].
TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) is produced both by decidual and trophoblast cells during pregnancy and known to participate in apoptosis. In this study, we aimed to determine and to compare maternal serum and placental TRAIL-R2 levels in patients with placenta accreta, non-adherent placenta previa and in healthy pregnancies. We also aimed to analyze the association of placenta accreta with the occurrence of previous C-sections.
A total of 82 pregnant women were enrolled in this case–control study (27 placenta accreta patients, 26 non-adherent placenta previa patients and 29 age-, and BMI-matched healthy, uncomplicated pregnant controls). TRAIL-R2 levels were studied in both maternal serum and placental tissue homogenates. Determining the best predictor(s) which discriminate placenta accreta was analyzed by multiple logistic regression analyses. Adjusted odds ratios and 95% confidence intervals were also calculated.
Both placental and serum TRAIL-R2 levels were significantly lower in placenta accreta group (median 34.82 pg/mg and 19.85 pg/mL, respectively) when compared with both non-adherent placenta previa (median 39.24 pg/mg and 25.99 pg/mL, respectively) and the control groups (median 41.62 pg/mg and 25.87 pg/mL, respectively) (p < 0.05). Placental TRAIL-R2 levels and previous cesarean section were found to be significantly associated with placenta accreta (OR: 0.934 95% CI 0.883–0.987, p = 0.016 and OR:7.725 95% CI: 2.717–21.965, p < 0.001, respectively). Placental and serum TRAIL-R2 levels were positively correlated.
Decreased levels of placental TRAIL-R2 and previous history of cesarean section were found to be significantly associated with placenta accreta, suggesting a possible role of apoptosis in abnormal trophoblast invasion.
Sexual Dimorphism and DOHaD through the Lens of Epigenetics: Genetic, Ancestral, Developmental, and Environmental Origins from Previous to the Next Generation(s)
2015, The Epigenome and Developmental Origins of Health and Disease
There is increasing interest in sex-specific nongenetic and noncultural mechanisms transferring a memory of parental exposure to various environments and determining the reactivity of subsequent generations to their environment during their lifetimes. The epigenetic origins of sexual dimorphism are due not only to the chromosomal sex (XX or XY) at conception prior to gonad differentiation, but later on, to a complex intermingling of both hormones and X and Y genes regulating autosomal genes. Sexual dimorphism may also date back to the sex of ancestors who experienced exposure to different environmental factors and transmitted their “imprint” in a sex-specific manner, either through the maternal or paternal lineage or both, and in a manner that may also depend on the sex of the offspring. Observed sexual dimorphism is the result of a subtle entanglement of different epigenetic and other factors and how and when early and life-long environmental exposures interact with them, leading to specific responses, outcomes, and persistence for men and women.
Miscellaneous Placental Pathology (Includes Massive Perivillous Fibrin Deposition, Fetal Thrombotic Vasculopathy, and Placenta Accreta)
2014, Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms
This article reviews the pathogenetic mechanisms of three important, but less common, placental pathologies. Maternal floor infarction and massive perivillous fibrin deposition are pathologically overlapping placental disorders with characteristic gross and shared light microscopic features of excessive perivillous deposition of fibrinoid material. While rare, they are important lesions to recognize, because they are associated with high rates of fetal growth restriction, perinatal morbidity and mortality, and risks of recurrence with fetal death. The cause of the extensive fibrinoid deposition in the maternal space is unknown, but evidence supports the involvement of maternal alloimmune or autoimmune mechanisms, at least in some cases. Fetal thrombotic vasculopathy (FTV) also represents an important constellation of pathological findings in the placenta characterized by fetal vascular thrombosis and loss of downstream villous vasculature. Oftentimes, the changes of FTV are associated with gross umbilical cord abnormalities and/or umbilical cord obstruction, but other conditions that promote vascular stasis, endothelial damage, or hypercoagulability can also be implicated in the pathogenesis. As will be discussed, FTV is associated with several important neonatal complications including neurological impairment. Placenta accreta is a pathological condition in which the placenta is adherent to the myometrium and is believed to occur most commonly secondary to defective decidualization of the endometrium. Placenta accreta is an important cause of serious obstetrical hemorrhage and is increasing in incidence secondary to the increased rates of delivery by cesarean section method. This article reviews the mechanisms of pathogenesis as well as gross and histological appearances of placenta accreta.
Trypanosoma cruzi induces trophoblast differentiation: A potential local antiparasitic mechanism of the human placenta?
2014, Placenta
The congenital transmission of Trypanosoma cruzi (T. cruzi) is responsible for one-third of new Chagas disease cases each year. During congenital transmission, the parasite breaks down the placental barrier formed by the trophoblast, basal laminae and villous stroma. The observation that only 5% of infected mothers transmit the parasite to the fetus implies that the placenta may impair parasite transmission. The trophoblast undergoes continuous epithelial turnover, which is considered part of innate immunity. Therefore, we propose that T. cruzi induces differentiation in the trophoblast as part of a local antiparasitic mechanism of the placenta.
We analyzed β-human chorionic gonadotropin (β-hCG) and syncytin protein expression in HPCVE and BeWo cells using immunofluorescence and western blotting. Additionally, β-hCG secretion into the culture medium was measured by ELISA. We assessed the differentiation of trophoblastic cells in BeWo cells using the two-color fusion assay and by determining desmoplakin re-distribution.
T. cruzi trypomastigotes induce β-hCG secretion and protein expression as well as syncyntin protein expression in HPCVE and BeWo cells. Addionally, the parasite induces the trophoblast fusion of BeWo cells.
T. cruzi induces differentiation of the trophoblast, which may contribute to increase the trophoblast turnover. The turnover could be a component of local antiparasitic mechanisms in the human placenta.
Placenta Accreta and Percreta
2013, Surgical Pathology Clinics
Citation Excerpt :
Placenta accreta associated with multiple cesarean sections has led to a markedly increased rate of peripartum hysterectomies,5 and the risk goes up with each additional cesarean section a woman undergoes.6 The origin of accreta after cesarean includes a defect in the decidua basalis as well as abnormal repair and vascularization.7 Some investigators have also suggested that accreta is more common when a single layer closure is used during previous cesarean sections.

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¹: GEL edited this manuscript based on contributions from the other authors.

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