IFPA meeting 2018 workshop report II: Abnormally invasive placenta; inflammation and infection; preeclampsia; gestational trophoblastic disease and drug delivery

doi:10.1016/j.placenta.2019.02.006

Placenta

Volume 84, 1 September 2019, Pages 9-13

https://doi.org/10.1016/j.placenta.2019.02.006 Get rights and content

Highlights

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Preeclampsia is secondary to trophoblast factors shed into the maternal circulation.
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No single imaging sign has been demonstrated to be diagnostic of abnormally invasive placenta.
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Timing of infection during pregnancy may be critical for impacting pregnancy outcomes.

Abstract

Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialized topics. At IFPA meeting 2018 there were nine themed workshops, five of which are summarised in this report. These workshops discussed new perspectives and knowledge in the following areas of research: 1) preeclampsia; 2) abnormally invasive placenta; 3) placental infection; 4) gestational trophoblastic disease; 4) drug delivery to treat placental dysfunction.

Section snippets

Preeclampsia and the placenta: what's new?

Chairs: Christopher Redman and Mitsutoshi Iwashita.

Speakers: Larry Chamley, Stephen Charnock-Jones, Akitoshi Nakashima, Manu Vatish.

Abnormally invasive placenta (AIP): an international perspective

Chairs: Sally Collins and Kiyotake Ichizuka.

Speakers: Sally Collins, Nicholas Illsley, Abdulla Al Khan, Kenji Tanimura.

Impact of infection on placental biology

Chairs: Gendie Lash and Shigeru Saito.

Speakers: Thaddeus Golos, Solene Grayo, Gendie Lash, Shigeru Saito, Kenji Tanimura, Bryce Wolfe.

Gestational trophoblastic disease (GTD)

Chairs: Kazuhiko Ino and Eiko Yamamoto.

Speakers: Hiroshi Fujiwara, Kaoru Niimi, Hirokazu Usui, Eiko Yamamoto.

Drug delivery in pregnancy: overcoming problems and developing new technologies

Chairs: Lynda Harris and Masatoshi Tomi.

Speakers: Natalie Hannan, Lynda Harris, Sampada Kallol (presented on behalf of Christiane Albrecht), Takeshi Nagamatsu, Masataka Nomoto, Masatoshi Tomi.

References (0)

Cited by (7)

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Our previous study has shown that maternal exposure to environmental pollutants DEHP during pregnancy induces fetal growth restriction by inhibiting the proliferation of placental cells through DNA damage [17]. Placental development defects are associated with fetal growth retardation, leading to adverse pregnancy outcomes and some diseases in adulthood of offsprings [39,40]. Therefore, it is very essential to understand the mechanism of DNA damage in placental cells treated by DEHP.
Di (2-ethyl-hexyl) phthalate (DEHP) is a wildly used plasticizer. Maternal exposure to DEHP during pregnancy blocks the placental cell cycle at the G2/M phase by reducing the efficiency of the DNA repair pathways and affects the health of offsprings. However, the mechanism by which DEHP inhibits the repair of DNA damage remains unclear. In this study, we demonstrated that DEHP inhibits DNA damage repair by reducing the activity of the DNA repair factor recruitment molecule PARP1. NAD⁺ and ATP are two substrates necessary for PARP1 activity. DEHP abated NAD⁺ in the nucleus by reducing the level of NAD⁺ synthase NMNAT1 and elevated NAD⁺ in the mitochondrial by promoting synthesis. Furthermore, DEHP destroyed the mitochondrial respiratory chain, affected the structure and quantity of mitochondria, and decreased ATP production. Therefore, DEHP inhibits PARP1 activity by reducing the amount of NAD⁺ and ATP, which hinders the DNA damage repair pathways. The supplement of NAD⁺ precursor NAM can partially rescue the DNA and mitochondria damage. It provides a new idea for the prevention of health problems of offsprings caused by DEHP injury to the placenta.
Di (2-ethyl-hexyl) phthalate disrupts placental growth in a dual blocking mode
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Citation Excerpt :
Together, these results indicate that in response to DNA DSB and excessive progesterone, trophoblast cells formed micronuclei to inhibit cell proliferation. The development of the placenta is affected by some exogenous chemicals, which might inhibit the growth of the fetus and be associated with some diseases in adulthood (Burton and Jauniaux, 2018; Albrecht et al., 2019). DEHP is an endocrine disrupter with genetic toxicity (Erkekoglu and Kocer-Gumusel, 2014; Erkekoglu et al., 2010; Chang et al., 2017).
Di (2-ethyl-hexyl) phthalate (DEHP) is a widely used plasticizer. Maternal DEHP exposure inhibits cell proliferation and reduces placentas size, which associates with fetal growth restriction and adulthood diseases. However, the mechanism of placental cell proliferation inhibition by DEHP remains elusive. This study investigated the effect of DEHP on placental cell proliferation from cell cycle arrest. Utilizing in vitro and in vivo experiments, we investigated cell cycle arrest, DNA double-strand break (DSB) repair, genotoxic stress response, and micronuclei formation. Most DEHP metabolizes to mono (2-Ethylhexyl) phthalate (MEHP) and distributes to organs quickly, so MEHP and DEHP were used in cultured cell and animal experiments, respectively. Here, a double blocking mode for the proliferation inhibition of the placental cell was revealed. One is that the classical DSB repair pathways were suppressed, which arrested the cell cycle at the G2/M phase. The other is that DEHP stimulated an elevated level of progesterone, which blocked the cell cycle at metaphase by disrupting chromosome arrangement. These two sets of events facilitated micronuclei formation and resulted in cell proliferation inhibition. This findings provide a novel mechanistic understanding for DEHP to inhibit placental cell proliferation.
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