Placental tryptophan metabolism as a potential novel pathway for the developmental origins of mental diseases

Goeden, Nick; Velasquez, Juan C.; Bonnin, Alexandre

doi:10.3402/tdp.v1i0.20593

Cited by 16 publications

(8 citation statements)

References 38 publications

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“…Reduced expression of Irs1 in OB dams could lead to insulin resistance in placental labyrinth and affect these processes. Finally, downregulation of Tph1 could impair the transformation of maternal tryptophan to serotonin, a process that is necessary for proper fetal brain development [ 49 , 50 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

et al. 2016

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BackgroundMaternal obesity impacts fetal growth and pregnancy outcomes. To counteract the deleterious effects of obesity on fertility and pregnancy issue, preconceptional weight loss is recommended to obese women. Whether this weight loss is beneficial/detrimental for offspring remains poorly explored. Epigenetic mechanisms could be affected by maternal weight changes, perturbing expression of key developmental genes in the placenta or fetus. Our aim was to investigate the effects of chronic maternal obesity on feto-placental growth along with the underlying epigenetic mechanisms. We also tested whether preconceptional weight loss could alleviate these effects.ResultsFemale mice were fed either a control diet (CTRL group), a high-fat diet (obese (OB) group), or a high-fat diet switched to a control diet 2 months before conception (weight loss (WL) group). At mating, OB females presented an obese phenotype while WL females normalized metabolic parameters. At embryonic day 18.5 (E18.5), fetuses from OB females presented fetal growth restriction (FGR; −13 %) and 28 % of the fetuses were small for gestational age (SGA). Fetuses from WL females normalized this phenotype. The expression of 60 epigenetic machinery genes and 32 metabolic genes was measured in the fetal liver, placental labyrinth, and junctional zone. We revealed 23 genes altered by maternal weight trajectories in at least one of three tissues. The fetal liver and placental labyrinth were more responsive to maternal obesity than junctional zone. One third (18/60) of the epigenetic machinery genes were differentially expressed between at least two maternal groups. Interestingly, genes involved in the histone acetylation pathway were particularly altered (13/18). In OB group, lysine acetyltransferases and Bromodomain-containing protein 2 were upregulated, while most histone deacetylases were downregulated. In WL group, the expression of only a subset of these genes was normalized.ConclusionsThis study highlights the high sensitivity of the epigenetic machinery gene expression, and particularly the histone acetylation pathway, to maternal obesity. These obesity-induced transcriptional changes could alter the placental and the hepatic epigenome, leading to FGR. Preconceptional weight loss appears beneficial to fetal growth, but some effects of previous obesity were retained in offspring phenotype.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0188-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

et al. 2016

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“…This phenomenon is also a known sign of other illnesses, for example, yellow fever. The tendency towards bradycardia is related to down-regulating IL-6 production by inhibiting two MyD88-dependent LPS signalling pathways (Figure 19 and Figure 20) [86][87][88].…”

Section: Figure 17mentioning

confidence: 99%

Untitled

2021

J Infect Dis Epidemiol

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“…The function of the placental microbiome is predicted to regulate tryptophan, fatty acid metabolism, and benzoate degradation. Placental tryptophan metabolism is known to be important for neurodevelopment of the fetus (37). Catabolism of tryptophan is linked to the creation of neurodevelopmental fetomaternal immune tolerance (84).…”

Section: The Normal Placental Microbiomementioning

confidence: 99%

Maternal microbiome and the hypertensive disorder of pregnancy, preeclampsia

Beckers

Sones

2020

American Journal of Physiology-Heart and Circulatory Physiology

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Preeclampsia (PE) is a pregnancy-specific disorder that can be life threatening for both mother and baby. It is characterized by a new onset hypertension during the second half of pregnancy and affects ~300,000 women in the United States every year. There is no cure for PE, and the only effective treatment is delivery of the placenta and the fetus, which is often preterm. PE is believed to be a severe manifestation of placental dysfunction due to early angiogenic imbalances and inflammatory disturbances; however, the cause of this is unknown. The once thought “sterile” placenta now has been proposed to have a unique microbiome of its own. Under ideal conditions, the microbiome represents a balanced bacterial community that is important to the maintenance of a healthy environment. Dysbiosis of these communities may lead to inflammation that potentially contributes to adverse pregnancy outcomes, such as preterm birth and PE. Thus far, the female reproductive tract microbiome has been found to be influenced by periodontal disease, cardiometabolic complications, and maternal obesity, all of which have been identified as contributors to PE. This review will look at the maternal reproductive tract microbiome, evidence for and against, and its role in pregnancy and PE-related events as well as data from relevant mouse models that could be useful for further investigating the influence of the reproductive tract microbiome on the pathogenesis of PE.

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Placental tryptophan metabolism as a potential novel pathway for the developmental origins of mental diseases

Cited by 16 publications

References 38 publications

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

Untitled

Maternal microbiome and the hypertensive disorder of pregnancy, preeclampsia

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