Fathers That Are Born Small Program Alterations in the Next-Generation Preimplantation Rat Embryos ,

Master, Jordanna S; Thouas, George Anthony; Harvey, Alexandra J; Sheedy, John R; Hannan, Natalie J.; Wlodek, Mary E.

doi:10.3945/jn.114.205724

Cited by 11 publications

(10 citation statements)

References 67 publications

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“…Along the same lines, Skjaerven et al 13 showed that daughters of pre-eclamptic mothers demonstrated an almost two-fold higher risk of developing pre-eclampsia compared with pregnancies fathered by sons of pre-eclamptic women. These findings are in line with experimental data suggesting that placenta-mediated diseases (mainly SGA and pre-eclampsia) are associated with genetic or epigenetic modifications that can be transmitted to the following generations via the maternal germ-cell line, an altered in-utero environment or by maternal mitochondrial DNA 10,15,[25][26][27] .…”

Section: Figuresupporting

confidence: 89%

Transgenerational transmission of small‐for‐gestational age

Bijnens

Rodríguez‐López

Miño

et al. 2019

Ultrasound in Obstet & Gyne

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Section: Figuresupporting

confidence: 89%

Transgenerational transmission of small‐for‐gestational age

Bijnens

Rodríguez‐López

Miño

et al. 2019

Ultrasound in Obstet & Gyne

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“…Cell counts were not different between sexes and were also similar to counts from Wistar rat embryos obtained at a similar time point [41]. Investigation of TE differentiation using culture of in vivo-derived embryos also showed no changes to outgrowth rate, number of trophoblasts, P-TGCs, ploidy or expression of TS and trophoblast differentiation markers.…”

Section: Discussionsupporting

confidence: 53%

Sex differences in rat placental development: from pre-implantation to late gestation

et al. 2017

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BackgroundA male fetus is suggested to be more susceptible to in utero and birth complications. This may be due in part to altered morphology or function of the XY placenta. We hypothesised that sexual dimorphism begins at the blastocyst stage with sex differences in the progenitor trophectoderm (TE) and its derived trophoblast lineages, as these cells populate the majority of cell types within the placenta. We investigated sex-specific differences in cell allocation in the pre-implantation embryo and further characterised growth and gene expression of the placental compartments from the early stages of the definitive placenta through to late gestation.MethodsNaturally mated Sprague Dawley dams were used to collect blastocysts at embryonic day (E) 5 to characterise cell allocation; total, TE, and inner cell mass (ICM), and differentiation to downstream trophoblast cell types. Placental tissues were collected at E13, E15, and E20 to characterise volumes of placental compartments, and sex-specific gene expression profiles.ResultsPre-implantation embryos showed no sex differences in cell allocation (total, TE and ICM) or early trophoblast differentiation, assessed by outgrowth area, number and ploidy of trophoblasts and P-TGCs, and expression of markers of trophoblast stem cell state or differentiation. Whilst no changes in placental structures were found in the immature E13 placenta, the definitive E15 placenta from female fetuses had reduced labyrinthine volume, fetal and maternal blood space volume, as well as fetal blood space surface area, when compared to placentas from males. No differences between the sexes in labyrinth trophoblast volume or interhaemal membrane thickness were found. By E20 these sex-specific placental differences were no longer present, but female fetuses weighed less than their male counterparts. Coupled with expression profiles from E13 and E15 placental samples may suggest a developmental delay in placental differentiation.ConclusionsAlthough there were no overt differences in blastocyst cell number or early placental development, reduced growth of the female labyrinth in mid gestation is likely to contribute to lower fetal weight in females at E20. These data suggest sex differences in fetal growth trajectories are due at least in part, to differences in placenta growth.Electronic supplementary materialThe online version of this article (doi:10.1186/s13293-017-0138-6) contains supplementary material, which is available to authorized users.

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“…We have published that preimplantation blastocysts derived from fathers born small are altered, highlighting a potential pathway to F2 offspring deficits and dysfunction (Master et al . ). Ng et al .…”

Section: Introductionmentioning

confidence: 97%

Programming of maternal and offspring disease: impact of growth restriction, fetal sex and transmission across generations

Cheong

Wlodek

Moritz

et al. 2016

The Journal of Physiology

125

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partly attributed to different placenta-regulated growth strategies of the male and female fetus. Pregnancy is known to be a major risk factor for unmasking a number of conditions and can be considered a 'second hit' for women who were born small. As such, female offspring often develop impairments of physiology for the first time during pregnancy that present as pregnancy complications. Numerous maternal stressors can further increase the risk of developing a maternal complication during pregnancy. Importantly, these maternal complications can have long-term consequences for both the mother after pregnancy and the developing fetus. Conditions such as preeclampsia, gestational diabetes and hypertension as well as thyroid, liver and kidney diseases are all conditions that can complicate pregnancy and have long-term consequences for maternal and offspring health. Babies born to mothers who develop these conditions are often at a greater risk of developing disease in adulthood. This has implications as a mechanism for transmission of disease across generations. In this review, we discuss the evidence surrounding long-term intergenerational implications of being born small and/or experiencing stress during pregnancy on programming outcomes. Abstract figure legend Sex-specific fetal programming and the transgenerational transmission of diseases. Perturbations of the fetal environment during critical periods of development can have many consequences in postnatal life. This is primarily regulated by the placenta, which is known to respond to stressful stimuli in a sex-specific manner. Individuals exposed to suboptimal conditions in utero are programmed for various diseases including cardiovascular and metabolic diseases. Females programmed during fetal life have increased risk of developing pregnancy complications. The germ cells of exposed individuals may also be compromised. Together, they contribute to an adverse fetal environment and places the next generation of offspring at risk of adverse health. Importantly, stress is known to exacerbate these programmed outcomes during fetal and postnatal life.

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Fathers That Are Born Small Program Alterations in the Next-Generation Preimplantation Rat Embryos ,

Cited by 11 publications

References 67 publications

Transgenerational transmission of small‐for‐gestational age

Transgenerational transmission of small‐for‐gestational age

Sex differences in rat placental development: from pre-implantation to late gestation

Programming of maternal and offspring disease: impact of growth restriction, fetal sex and transmission across generations

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