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Placental-Liver Crosstalk in the Control of Pregnancy

ABSTRACT: Placental-Liver Crosstalk in the Control of Pregnancy

PROVIDER: PRJEB50835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR8528930.fastq.gz	Fastqsanger.gz
	ERR8528931.fastq.gz	Fastqsanger.gz
	ERR8528932.fastq.gz	Fastqsanger.gz
	ERR8528933.fastq.gz	Fastqsanger.gz
	ERR8528934.fastq.gz	Fastqsanger.gz

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Placental-Liver Crosstalk in the Control of Pregnancy

Project description:The placenta is a potent endocrine organ that secretes hormones with metabolic effects into maternal circulation. On the other hand, the liver, which is the main detoxification organ of the body, plays a key role in regulating maternal glucose and insulin metabolism during pregnancy. Failures in the production of placental hormones and/or the liver to adapt its structure and function to pregnancy can result in metabolic diseases such as gestational diabetes. Previous work has shown that the imprinted Igf2-H19 locus is involved in controlling placental endocrine function in mice. This study used conditional mis-expression of the Igf2-H19 locus to induce placental endocrine malfunction and study its consequences on hepatic gene regulation during pregnancy.

2024-11-27 | E-MTAB-11439 | biostudies-arrayexpress

Placental changes caused by food restriction during early pregnancy in mice are reversible

Project description:In a previous study, 50% calorie restriction in mice from days 1.5-11.5 of pregnancy resulted in reduced placental weights and areas, relatively sparing of labyrinth zone area compared to junctional zone area, and dramatic changes in global gene expression profiles. Here we examined placental gene expression at day 18.5, after the return to normal feeding to see whether differences were reversible Mice were randomized to 2 treatment groups on day 1.5 of pregnancy: (1) ad libitum fed (control) (2) 50% food restriction (restricted). Mice were returned to ad libitum feed on d11.5, sacrificed on d18.5 and placentas were collected.

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Project description:The placenta acts as an interface between the mother and fetus, regulating nutrient transport and secreting hormones which impact maternal metabolism. Complications during pregnancy, such as placental endocrine malfunction, programme offspring to develop metabolic disease during adulthood, in part via changes in gene expression in critical metabolic organs, such as the liver, during fetal development. Placental endocrine malfunction was induced via the misexpression of two imprinted genes (Igf2 and H19) exclusively in the endocrine zone of the mouse placenta, to study the consequences this has on fetal hepatic gene expression.

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Project description:We hypothesized that the trophoblast secretes anti-angiogenic factors, which increase in late pregnancy to limit angiogenesis. Therefore, we determined the paracrine effect of primary human trophoblasts from early versus late pregnancy on the angiogenic potential of isolated feto-placental endothelial cells. We found that the expression and secretion of anti-angiogenic factors differs in early vs late pregnancy, and differentially affects feto-placental angiogenesis.

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Maternal pre-pregnancy obesity is associated with altered placental transcriptome

Project description:Maternal obesity is becoming a major health consideration for successful pregnancy outcomes. There is growing proof that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are so far poorly understood. We set out to analyse term placenta whole transcriptome in obese (n=5) and normoweight women (n=5), using Affymetrix microarray platform compromising of 50,000 probe sets. Our analysis shows that the placental transcriptome differs between normoweight and obese women. Different processes and pathways among placenta from obese women were dysregulated, including inflammation and immune responses, lipid metabolism, cell death and survival and cancer pathways, vasculogenesis and angiogenesis, and glucocorticoid receptor signaling pathway. Together, this global gene expression profiling approach demonstrates and confirms that maternal obesity creates a unique in utero environment that impairs placental transcriptome.

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Project description:The human placenta is a rapidly developing organ with a relatively short life span that performs multiple functions until birth. Investigations into molecular mechanisms that control placental plasticity during its maturation might be useful in understanding patho-physiology of pregnancy-specific disorders. We hypothesized that molecular rearrangements and phenotypic adaptations that are necessary for normal placental development and maturation are reflected in its genotype. Our objective was to investigate global gene expression profile in the first and third trimester normal human placentas. 21 women were recruited with uncomplicated pregnancies that were delivered at term and 16 healthy women undergoing surgical abortion at 9-12 weeks gestation. We compared global placental gene expression profile by Human Genome Survey Microarray v.2.0 (Applied Biosystems). A total of 37 hybridisations were performed applying direct comparison design.

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Placental uptake and metabolism as determinants of pregnancy vitamin D status [Array]

Project description:Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.

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