Genistein upregulates placental corticotropin-releasing hormone expression in lipopolysaccharide-sensitized mice

Huang, Hui; Li, L.; Wang, Y.; Tang, Ling; Wang, C.C.; Leung, Lai K.

doi:10.1016/j.placenta.2011.07.082

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…) and mouse placenta (Huang et al . ), with changes in mouse placental mRNA levels being reflected in maternal circulating plasma CRH. The current study showed that while hypoxia did not influence Crh mRNA levels, Crh mRNA was higher in males compared to females.…”

Section: Discussionmentioning

confidence: 99%

Mid‐ to late term hypoxia in the mouse alters placental morphology, glucocorticoid regulatory pathways and nutrient transporters in a sex‐specific manner

Cuffe

Walton

Singh

et al. 2014

The Journal of Physiology

115

168

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Key pointsr Maternal hypoxia is a common perturbation that may impair fetal development and programme sex specific disease outcomes in offspring.r There is growing interest in the role of the placenta in mediating the effects of maternal hypoxia on fetal development, particularly in late gestation during maximal fetal growth.r Multiple mechanisms have been proposed to play a role in hypoxia induced impairment of placental development. Here we investigated the role of glucocorticoids and glucose regulation.r This study shows that fetal sex determines placental adaptations to maternal hypoxia: while maternal hypoxia increased maternal glucose and corticosterone levels in both sexes, placental adaptations to impaired maternal physiology were more evident in female fetuses, in which factors responsible for the regulation of glucocorticoids and nutrient transport were most severely affected by maternal hypoxia.Abstract Maternal hypoxia is a common perturbation that can disrupt placental and thus fetal development, contributing to neonatal impairments. Recently, evidence has suggested that physiological outcomes are dependent upon the sex of the fetus, with males more susceptible to hypoxic insults than females. This study investigated the effects of maternal hypoxia during midto late gestation on fetal growth and placental development and determined if responses were sex specific. CD1 mice were housed under 21% or 12% oxygen from embryonic day (E) 14.5 until tissue collection at E18.5. Fetuses and placentas were weighed before collection for gene and protein expression and morphological analysis. Hypoxia reduced fetal weight in both sexes at E18.5 by 7% but did not affect placental weight. Hypoxia reduced placental mRNA levels of the mineralocorticoid and glucocorticoid receptors and reduced the gene and protein expression of the glucocorticoid metabolizing enzyme HSD11B2. However, placentas of female fetuses responded differently to maternal hypoxia than did placentas of male fetuses. Notably, morphology was significantly altered in placentas from hypoxic female fetuses, with a reduction in placental labyrinth blood spaces. In addition mRNA expression of Glut1, Igf2 and Igf1r were reduced in placentas of female fetuses only. In summary, maternal hypoxia altered placental formation in a sex specific manner through mechanisms involving placental vascular development, growth factor and nutrient transporter expression and placental glucocorticoid signalling. This study provides insight into how sex differences in offspring disease development may be due to sex specific placental adaptations to maternal insults. Abbreviations Crh, corticotropin releasing hormone; Crhr1, corticotropin releasing hormone receptor 1; E, embryonic day; Flt1, Fms related tyrosine kinase 1; Glut1, glucose transporter 1; Glut3, glucose transporter 3; Hif1a, hypoxia inducible factor 1 alpha; Hsd11b2, 11 beta hydroxysteroid dehydrogenase type 2; Igf2, insulin like growth factor 2; Igf1r, insulin like growth factor 1 receptor; Igf2r, Insulin like g...

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Section: Discussionmentioning

confidence: 99%

Mid‐ to late term hypoxia in the mouse alters placental morphology, glucocorticoid regulatory pathways and nutrient transporters in a sex‐specific manner

Cuffe

Walton

Singh

et al. 2014

The Journal of Physiology

115

168

View full text Add to dashboard Cite

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“…Lipopolysaccharide (LPS) endotoxin may induce premature birth in rodents. LPS treatment increases the incidence of early delivery in pregnant mice; the co‐administration of genistein and LPS induces high expression of placental corticotropin‐releasing hormone (CHR), indicating that genistein might exacerbate the undesirable effect of LPS on pregnant mice . Currently, there are no clear answers regarding the effects of phytoestrogens on human health.…”

Section: Dietary Polyphenolsmentioning

confidence: 99%

Management of reproduction and pregnancy complications in maternal obesity: Which role for dietary polyphenols?

et al. 2013

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Obesity is a global and dramatic public health problem; maternal obesity represents one of the main risk factors of infertility and pregnancy complications as it is associated with adverse maternal and offspring outcomes. In the last few years, adipose tissue dysfunction associated with altered adipocytokine secretion has been suggested to play a critical role in all the phases of reproductive process. Obesity is a nutrition-related disorder. In this regard, dietary intervention strategies, such as high intake of fruit and vegetables, have shown significant effects in both preserving health and counteracting obesity-associated diseases. Evidence has been provided that polyphenols, important constituents of plant-derived food, can influence developmental program of oocyte and embryo, as well as pregnancy progression by modulating several cellular pathways. This review will examine the controversial results so far obtained on adipocytokine involvement in fertility impairment and pregnancy complications. Furthermore, the different effects exerted by polyphenols on oocyte, embryo, and pregnancy development will be also taken in account.

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“…In rodents, placental CRH mRNA has also been reported (23,24). It has been shown that neurogenesis, neuron functioning, and cell survival in the hippocampus are affected by MIA (25)(26)(27).…”

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confidence: 98%

Sex-specific gene–environment interactions underlying ASD-like behaviors

Schaafsma

Gagnidze

Reyes

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

106

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The male bias in the incidence of autism spectrum disorders (ASDs) is one of the most notable characteristics of this group of neurodevelopmental disorders. The etiology of this sex bias is far from known, but pivotal for understanding the etiology of ASDs in general. Here we investigate whether a "three-hit" (genetic load × environmental factor × sex) theory of autism may help explain the male predominance. We found that LPS-induced maternal immune activation caused male-specific deficits in certain social responses in the contactin-associated protein-like 2 (Cntnap2) mouse model for ASD. The three "hits" had cumulative effects on ultrasonic vocalizations at postnatal day 3. Hits synergistically affected social recognition in adulthood: only mice exposed to all three hits showed deficits in this aspect of social behavior. In brains of the same mice we found a significant three-way interaction on corticotropin-releasing hormone receptor-1 (Crhr1) gene expression, in the left hippocampus specifically, which co-occurred with epigenetic alterations in histone H3 N-terminal lysine 4 trimethylation (H3K4me3) over the Crhr1 promoter. Although it is highly likely that multiple (synergistic) interactions may be at work, change in the expression of genes in the hypothalamic-pituitary-adrenal/ stress system (e.g., Crhr1) is one of them. The data provide proof-of-principle that genetic and environmental factors interact to cause sex-specific effects that may help explain the male bias in ASD incidence.maternal immune activation | prenatal stress | sex differences | Cntnap2 | autism A utism spectrum disorders (ASDs) comprise a heterogeneous group of neurodevelopmental disorders. The core symptoms of ASD are deficits in social communication and social interactions (Diagnostic and Statistical Manual of Mental Disorders V) and one of the most noticeable biological constants in this group of disorders is the sex difference: ∼80% of the children diagnosed with an ASD are boys (1). Many genes have been implicated in the etiologies underlying ASD in humans and ASD-like behavior in animal models. Some of these genes are located on the sex chromosomes and many of these genes may be able to affect other sex-chromosomal genes or may otherwise indirectly lead to sex-specific effects (reviewed in ref.2). However, it seems unlikely that these genes can account for the full sex bias in incidence and it is becoming increasingly clear that environmental factors play a very important role as well (3), and that these factors can interact with one another (2, 4). Moreover, prenatal testosterone (an indirect genetic factor) affects human behavior (5, 6) and may increase the risk to develop an ASD (7).Although today it is commonly proposed that many neurodevelopmental disorders result from interactions between "nature" and "nurture," studies investigating the gene-environment interaction in the development of ASD are scarce.In this study we tested whether an interaction between an ASD-related genetic mutation and an environmental factor may be a...

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Genistein upregulates placental corticotropin-releasing hormone expression in lipopolysaccharide-sensitized mice

Cited by 7 publications

References 34 publications

Mid‐ to late term hypoxia in the mouse alters placental morphology, glucocorticoid regulatory pathways and nutrient transporters in a sex‐specific manner

Mid‐ to late term hypoxia in the mouse alters placental morphology, glucocorticoid regulatory pathways and nutrient transporters in a sex‐specific manner

Management of reproduction and pregnancy complications in maternal obesity: Which role for dietary polyphenols?

Sex-specific gene–environment interactions underlying ASD-like behaviors

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